Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Showing posts with label memantine. Show all posts
Showing posts with label memantine. Show all posts

Saturday, April 19, 2025

Neurostimulant Use for Rehabilitation and Recovery After Stroke: A Narrative Literature Review

 I see nothing here that even remotely states what should be done to get recovered! You got published but DID NOTHING for getting survivors recovered!

Neurostimulant Use for Rehabilitation and Recovery After Stroke: A Narrative Literature Review

  • Abstract

    BACKGROUND:

    Stroke often results in significant impairments across various domains, including movement, language, cognition, and mood. Neurostimulants have been proposed as potential therapeutic interventions to enhance recovery in these areas.

    METHODS:

    This narrative literature review examines clinical trials investigating the efficacy of neurostimulants in poststroke recovery. It evaluates outcomes related to aphasia, motor deficits, cognition, fatigue, and depression.

    RESULTS:

    The qualitative analysis included 34 trials testing the following neurostimulants: methylphenidate (n=6), amphetamines (n=8), memantine (n=2), modafinil (n=2), levodopa (n=14), amantadine (n=1), bromocriptine (n=3), and ropinirole (n=1). Of the 34 studies, 31 were randomized, placebo-controlled (double-blind, n=27; single-blind, n=2; unblinded n=2), 2 were randomized and not placebo-controlled, and 1 was not randomized. Study design was either multiarm (n=23), crossover (n=10), or used subjects as their own control (n=1). Mean sample size was 49.4 (5–593).

    CONCLUSIONS:

    Current evidence suggests that memantine may be effective for aphasia, although few phase III trials exist, whereas bromocriptine and amphetamines lack sufficient evidence for long-term recovery of aphasia. Levodopa may improve motor aphasias but has not shown long-term benefits for motor recovery. Similarly, ropinirole has not been shown to improve poststroke motor outcomes. Methylphenidate has limited efficacy for cognitive improvement but may enhance poststroke functionality and mood. Modafinil may help with poststroke fatigue. In conclusion, there are promising results of positive effects of neurostimulants with few side effects, though studies are limited by heterogeneous designs and small sample sizes. Neurostimulant efficacy must be assessed in conjunction with specific rehabilitation modalities as part of larger, well-designed studies to best understand their effects on impairment.

    Graphical Abstract




    Get full access to this article

    Wednesday, August 28, 2019

    Paired Associative Stimulation as a Tool to Assess Plasticity Enhancers in Chronic Stroke

    Stroke survivors don't need lazy 'assessments' of MEP(Motor Evoked Potentials). Neither get you recovered! We need protocols. WHEN THE HELL WILL YOU GET THERE?

    Paired Associative Stimulation as a Tool to Assess Plasticity Enhancers in Chronic Stroke

    Joshua Silverstein1, Mar Cortes2, Katherine Zoe Tsagaris1, Alejandra Climent3, Linda M. Gerber4, Clara Oromendia4, Pasquale Fonzetti5,6, Rajiv R. Ratan5,7,8, Tomoko Kitago1,5*, Marco Iacoboni9,10, Allan Wu10,11, Bruce Dobkin12 and Dylan J. Edwards13,14
    • 1Human Motor Recovery Laboratory, Burke Neurological Institute, White Plains, NY, United States
    • 2Department of Rehabilitation and Human Performance, Icahn School of Medicine at Mount Sinai, New York, NY, United States
    • 3Sant Joan de Deu Hospital, Department of Neurology, University of Barcelona, Barcelona, Spain
    • 4Department of Healthcare Policy and Research, Weill Cornell Medical College, New York, NY, United States
    • 5Department of Neurology, Weill Cornell Medical College, New York, NY, United States
    • 6Memory Evaluation and Treatment Service, Burke Rehabilitation Hospital, White Plains, NY, United States
    • 7Burke Neurological Institute, White Plains, NY, United States
    • 8Feil Family Brain and Mind Research Institute, Weill Cornell Medical College, New York, NY, United States
    • 9Department of Psychiatry and Biobehavioral Sciences, UCLA Semel Institute for Neuroscience and Human Behavior, Los Angeles, CA, United States
    • 10Ahmanson-Lovelace Brain Mapping Center, University of California, Los Angeles, Los Angeles, CA, United States
    • 11Department of Neurology, University of California, Los Angeles, Los Angeles, CA, United States
    • 12Department of Neurology, Geffen School of Medicine, Reed Neurologic Research Center, University of California, Los Angeles, Los Angeles, CA, United States
    • 13Moss Rehabilitation Research Institute, Elkins Park, PA, United States
    • 14School of Medical and Health Sciences, Edith Cowan University, Perth, WA, Australia
    Background and Purpose: The potential for adaptive plasticity in the post-stroke brain is difficult to estimate, as is the demonstration of central nervous system (CNS) target engagement of drugs that show promise in facilitating stroke recovery. We set out to determine if paired associative stimulation (PAS) can be used (a) as an assay of CNS plasticity in patients with chronic stroke, and (b) to demonstrate CNS engagement by memantine, a drug which has potential plasticity-modulating effects for use in motor recovery following stroke.
    Methods: We examined the effect of PAS in fourteen participants with chronic hemiparetic stroke at five time-points in a within-subjects repeated measures design study: baseline off-drug, and following a week of orally administered memantine at doses of 5, 10, 15, and 20 mg, comprising a total of seventy sessions. Each week, MEP amplitude pre and post-PAS was assessed in the contralesional hemisphere as a marker of enhanced or diminished plasticity. Strength and dexterity were recorded each week to monitor motor-specific clinical status across the study period.
    Results: We found that MEP amplitude was significantly larger after PAS in baseline sessions off-drug, and responsiveness to PAS in these sessions was associated with increased clinical severity. There was no observed increase in MEP amplitude after PAS with memantine at any dose. Motor threshold (MT), strength, and dexterity remained unchanged during the study.
    Conclusion: Paired associative stimulation successfully induced corticospinal excitability enhancement in chronic stroke subjects at the group level. However, this response did not occur in all participants, and was associated with increased clinical severity. This could be an important way to stratify patients for future PAS-drug studies. PAS was suppressed by memantine at all doses, regardless of responsiveness to PAS off-drug, indicating CNS engagement.

    Introduction

    The capacity of the brain to make structural, physiological, and genetic adaptations following stroke, otherwise known as plasticity, is likely to be critical for improving sensorimotor impairments and functional activities. Promotion of adaptive plasticity in the central nervous system (CNS) leading to sustained functional improvement is of paramount importance, given the personal suffering and cost associated with post-stroke disability (Ma et al., 2014). In addition to rehabilitation therapies to retrain degraded motor skills, animal and human studies have tried to augment recovery with neuropharmacologic interventions. Unfortunately, few if any have had a notable effect in patients or have come into routine use (Martinsson et al., 2007; Chollet et al., 2011; Cramer, 2015; Simpson et al., 2015). Methods to screen drugs based on their presumed mechanism of action on plasticity in human motor systems could speed translation to patients. However, there is currently no accepted method in stroke patients for evaluating the potential effectiveness or individual responsiveness to putative “plasticity enhancing” drugs in an efficient, low-cost, cross-sectional manner, in order to establish target engagement in humans and to avoid the extensive time and cost of protracted clinical trials.
    Paired associative stimulation (PAS) is a safe, painless, and non-invasive technique known to result in short-term modulation of corticospinal excitability in the adult human motor system, lasting ∼90 min (Stefan et al., 2000; Wolters et al., 2003). Post-PAS excitability enhancement has been considered an LTP-like response thought to relate to transient changes in synaptic efficacy in the glutamatergic system at the N-methyl-D-aspartate (NMDA) receptor, since both human NMDA receptor deficiency (Volz et al., 2016) and pharmacological manipulation with dextromethorphan (Stefan et al., 2002) can block the effect. While PAS has been explored as a potential therapeutic intervention in patients with residual motor deficits after stroke (Jayaram and Stinear, 2008; Castel-Lacanal et al., 2009), it has not previously been investigated for its potential use as an assay of motor system plasticity in this context. Prior studies have suggested that motor practice and PAS share the same neuronal substrates, modulating LTP and LTD-like plasticity in the human motor system (Ziemann et al., 2004; Jung and Ziemann, 2009); therefore, as an established non-invasive human neuromodulation method (Suppa et al., 2017), we reasoned that PAS would be a suitable assay in the present study to examine the effect of a drug on motor system plasticity.
    Here, we examine the effect of memantine, a drug used for treatment of Alzheimer’s disease, on the PAS response in patients with chronic stroke. Memantine is described pharmacologically as a low affinity, voltage dependent, non-competitive, NMDA antagonist (Rogawski and Wenk, 2003). At high concentrations, like other NMDA-R antagonists, it can inhibit synaptic plasticity. At lower, clinically relevant concentrations, memantine can, under some circumstances, promote synaptic plasticity by selectively inhibiting extra-synaptic glutamate receptor activity while sparing normal synaptic transmission, and hence may have clinical utility for rehabilitation (Xia et al., 2010). Interest in specifically using the drug for its interaction with stroke pathophysiology stems from animal models of both prevention (Trotman et al., 2015), in which pre-conditioning reduced infarct size, as well as for functional recovery, in which chronic oral administration starting >2 h post-stroke resulted in improved function through a non-neuroprotective mechanism (López-Valdés et al., 2014). In humans, memantine taken over multiple days has been used to demonstrate that the NMDA receptor is implicated in specific transcranial magnetic paired-pulse measures (Schwenkreis et al., 1999), and short-term training-induced motor map reorganization (Schwenkreis et al., 2005). In studies of neuromodulation, memantine blocked the facilitatory effect of intermittent theta-burst stimulation (iTBS) (Huang et al., 2007). Similarly, LTP-like plasticity induced by associative pairing of painful laser stimuli and TMS over primary motor cortex (M1) can also be blocked by memantine (Suppa et al., 2013). The effects of memantine on the PAS response have not yet been demonstrated, including examination of potential dose-response effects, which would be important for the potential clinical application of memantine for stroke recovery.
    In our study, we set out to determine whether PAS might be a useful tool to probe the potential for plasticity after stroke in persons with chronic hemiparesis and apply PAS as an assay to look at drug effects on motor system plasticity using memantine. We hypothesized that (a) PAS would enhance corticospinal excitability in the contralesional hemisphere of stroke patients, and that (b) since PAS-induced plasticity is thought to involve a short-term change in glutamatergic synaptic efficacy, memantine would have a dose-dependent effect on PAS response. We predicted that at low doses, memantine would enhance PAS-induced plasticity through selective blockade of extrasynaptic NMDA receptors, whereas higher doses would inhibit PAS-induced plasticity.


    More at link.  

    Wednesday, May 29, 2019

    Memantine Improves Lewy Body Dementia & Parkinson's

    You might want to remember this because of your chance of getting Parkinsons.

    Parkinson’s Disease May Have Link to Stroke March 2017

     

    Memantine Improves Lewy Body Dementia & Parkinson's 

    Memantine (Namenda / Ebixa) is FDA-approved for Alzheimer's. Learn how it significantly improves memory and attention in Lewy Body Disease, Parkinson's and various types of dementia.



    An important study shows that performance on objective tests of attention and memory can be improved by memantine in two other major forms of dementia - Parkinson's disease dementia and dementia with Lewy Bodies. The improvements detected were highly statistically reliable and of clinically relevant effect sizes; indicating that memantine can produce cognitive benefits in patients with these dementias which match those seen previously with anticholinesterases.

    Memantine is FDA approved just for Alzheimer's. Doctors may prescribe it "off-label", if in their clinical judgment it may help their patient with Lewy Body dementia or Parkinson's disease.

    Both studies utilised the CDR System™, an automated cognitive test system, making a strong case for benefits for the increased sensitivity and specificity that such procedures bring to dementia research, when compared with the traditional tests which have been historically employed.

    The results were part of a presentation at the last Alzheimer's Association International Conference.

    The current consensus guidelines for diagnosis of dementia with Lewy Bodies (DLB) and Parkinson's disease dementia (PDD) identify deficits to attention as core features in both conditions. (2,3). The present study evaluated the effects of memantine in DLB & PDD.

    In related trials to date in both dementias, the CDR System has detected significant benefits with rivastigmine on various aspects of attention (4-7).

    METHODS

    1. This was a parallel group, double-blind, placebo controlled, multicentre trial of memantine
    2. 21 DLB and 30 PDD patients were assessed prior to dosing and again at 12 and 24 weeks
    3. CDR System tests of attention (simple and choice reaction time) and word recognition (immediate and delayed) were administered.
    4. The tasks were secondary measures and not included in the original study publication (8).

    RESULTS

    • Compared to placebo, memantine significantly improved choice reaction time (CRT) and the accuracy of both immediate and delayed word recognition (all p<0.02); with Cohen's d effect sizes of between 0.56 and 0.57.
    • The improvement in CRT was accompanied by a trend for improved accuracy on the task, and speed was numerically improved with memantine on the word recognition tasks.
    • Beneficial effects of memantine were seen on 3 of the 4 tasks used in this study.

    These are the first therapeutic improvements with memantine having clinically relevant effect sizes in either DLB or PDD on validated automated cognitive tests of attention and episodic recognition memory. They directly support the improvement in the primary study outcome. Every measure from every CDR System test moved in the direction of improvement with memantine.

    The analysis models included a term for the interaction between type of dementia with effects of treatment, but none of these approached significance for any measure. Thus the improvements with memantine occurred in both DLB and PDD.

    REFERENCES
    1.
    Ballard CG, Aarsland D, McKeith IG et al. Fluctuations in attention: PD dementia vs. DLB with Parkinsonism. Neurology 2002; 59: 1714-1720.
    2.
    McKeith IG, Dickson DW, Lowe J. Diagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium. Neurology 2005; 65: 1863–1872.
    3.
    Emre M, Aarsland D, Brown R et al. Clinical Diagnostic Criteria for Dementia Associated with Parkinson's Disease. Movement Disorders 2007; 22: 1689-1707.
    4.
    McKeith IG, Del Ser T, Spano P, et al. Efficacy of rivastigmine in dementia with Lewy bodies: a randomised, double-blind, placebo-controlled international study. Lancet 2000; 356: 2031-2036.
    5.
    Wesnes KA, McKeith IG, Ferrara R et al. Effects of rivastigmine on cognitive function in dementia with Lewy bodies: a randomised placebo-controlled international study using the Cognitive Drug Research computerised assessment System. Dementia and Geriatric Cognitive Disorders 2002; 13: 183-192.
    6.
    Emre M, Aarsland D, Albanese A et al. Rivastigmine for dementia associated with Parkinson's disease. The New England Journal of Medicine 2004; 351: 2509-2518.
    7.
    Wesnes KA, McKeith IG, Edgar C et al. Benefits of rivastigmine on attention in dementia associated with Parkinson disease. Neurology 2005; 65: 1654-1656.
    8.
    Aarsland D, Ballard C, Walker Z et al. Memantine in patients with Parkinson's disease dementia or dementia with Lewy bodies: a double-blind, placebo-controlled, multicentre trial. Lancet Neurology 2009; 8: 613–618.

    At baseline, compared to healthy age-matched controls the patients showed the previously identified characteristic profile of attentional impairment; as well as large effect sized deficits to CRT and the recognition accuracy scores.

    Wednesday, May 8, 2019

    Using Memantine to Prevent Alzheimer's

    With your very likely chance of getting dementia your doctor, if any good at all, will be following this closely. OR, you could train them.

    Your chances of getting dementia.

    1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.

    2. Then this study came out and seems to have a range from 17-66%. December 2013.

    3. A 20% chance in this research.   July 2013.

    4. Dementia Risk Doubled in Patients Following Stroke September 2018

     

    Using Memantine to Prevent Alzheimer's 

    MEDICATION --- NAMENDA® / EBIXA® (generic MEMANTINE) is FDA-approved for Alzheimer's. Learn about new research on how it may help in preventing or slowing dementia.



    The molecular processes that lead to Alzheimer's begin years before symptoms appear. Researchers have now found that an FDA-approved drug, memantine, currently used only for alleviating the symptoms of moderate-to-severe Alzheimer’s disease, might be used to prevent or slow the progression of the disease if used before those symptoms appear. The research also offers, based on extensive experimentation, a hypothesis as to why this might work.

    The findings are published currently online in the journal Alzheimer’s & Dementia.

    Prevent it from starting in the first place

    “Based on what we’ve learned so far, it is my opinion that we will never be able to cure Alzheimer’s disease by treating patients once they become symptomatic,” said George Bloom, a UVA professor and chair of the Department of Biology, who oversaw the study in his lab. “The best hope for conquering this disease is to first recognize patients who are at risk, and begin treating them prophylactically with new drugs and perhaps lifestyle adjustments that would reduce the rate at which the silent phase of the disease progresses.

    “Ideally, we would prevent it from starting in the first place.”

    Brain Neurons Attempt to Divide

    As Alzheimer’s disease begins, there is a lengthy period of time, perhaps a decade or longer, when brain neurons affected by the disease attempt to divide, possibly as a way to compensate for the death of neurons. This is unusual in that most neurons develop prenatally and then never divide again. But in Alzheimer’s the cells make the attempt, and then die.


    George Bloom’s lab specializes in understanding the biochemical changes that lead to Alzheimer’s disease. (Photo by Dan Addison, University Communications)
    “It’s been estimated that as much as 90 percent of neuron death that occurs in the Alzheimer’s brain follows this cell cycle reentry process, which is an abnormal attempt to divide,” Bloom said. “By the end of the course of the disease, the patient will have lost about 30 percent of the neurons in the frontal lobes of the brain.”

    Memantine blocks cell cycle reentry

    Erin Kodis, a former Ph.D. student in Bloom’s lab and now a scientific editor at AlphaBioCom, hypothesized that excess calcium entering neurons through calcium channels on their surface drive those neurons back into the cell cycle. This occurs before a chain of events that ultimately produce the plaques found in the Alzheimer’s brain. Several experiments by Kodis ultimately proved her theory correct.

    The building blocks of the plaques are a protein called amyloid beta oligomers. Kodis found that when neurons are exposed to toxic amyloid oligomers, the channel, called the NMDA receptor, opens, thus allowing the calcium flow that drives neurons back into the cell cycle.

    Memantine blocks cell cycle reentry by closing the NMDA receptor, Kodis found.

    Giving Memantine Long Before Symptoms

    “The experiments suggest that memantine might have potent disease-modifying properties if it could be administered to patients long before they have become symptomatic and diagnosed with Alzheimer’s disease,” Bloom said. “Perhaps this could prevent the disease or slow its progression long enough that the average age of symptom onset could be significantly later, if it happens at all.” Print Friendly Version of this pagePrint Get a PDF version of this webpagePDF

    Side Effects are Modest

    Side effects of the drug appear to be infrequent and modest.

    Bloom said potential patients would need to be screened for Alzheimer’s biomarkers years before symptoms appear. Selected patients then would need to be treated with memantine, possibly for life, in hopes of stopping the disease from ever developing, or further developing.

    Not to Raise False Hopes

    “I don’t want to raise false hopes,” Bloom said, but “if this idea of using memantine as a prophylactic pans out, it will be because we now understand that calcium is one of the agents that gets the disease started, and we may be able to stop or slow the process if done very early.”

    Bloom currently is working with colleagues at the UVA School of Medicine to design a clinical trial to investigate the feasibility of using memantine as an early intervention.



    Tuesday, August 7, 2018

    Existing drug may prevent Alzheimer's - memantine

    Since you have a pretty good chance of getting Alzheimers you'll have to ask your doctor what is the criteria/protocol for getting this drug as a preventative? Or is your doctor sitting on his/her ass waiting for SOMEONE ELSE TO SOLVE THE PROBLEM?

    Your chances of getting dementia.

    1. A documented 33% dementia chance post-stroke from an Australian study?   May 2012.
    2. Then this study came out and seems to have a range from 17-66%. December 2013.
    3. A 20% chance in this research.   July 2013.

    Existing drug may prevent Alzheimer's - mematine

    Healthline/Medical News Today | August 06, 2018
    Emerging evidence suggests that a "potent" drug could prevent the development of Alzheimer's disease—but only if a person takes the medication long before symptoms of this condition make an appearance.
    Alzheimer's disease is the most common form of dementia; according to the Centers for Disease Control and Prevention (CDC), an estimated 5.7 million adults in the United States live with this condition.
    Unfortunately, there is no cure for Alzheimer's, and following disease onset, symptoms tend to worsen progressively.
    Then, the question, "Can specialists prevent the disease in people deemed at increased risk?" arises.
    The authors of a new study, from the University of Virginia in Charlottesville, suggest that one drug called memantine—which is currently used to manage Alzheimer's symptoms—may actually help prevent the disease. This, however, might only happen if a person takes the drug before symptoms set in.
    "Based on what we've learned so far, it is my opinion that we will never be able to cure Alzheimer's disease by treating patients once they become symptomatic," says Professor George Bloom, of the University of Virginia, who oversaw the study.

    "The best hope for conquering this disease is to first recognize patients who are at risk, and begin treating them prophylactically with new drugs and perhaps lifestyle adjustments that would reduce the rate at which the silent phase of the disease progresses," he says, adding, "Ideally, we would prevent it from starting in the first place."

    The journal Alzheimer's & Dementia has now published the team's findings.

    The cell cycle re-entry process

    The researchers explain that Alzheimer's disease actually begins long before symptoms start to show—perhaps even a decade or longer in advance.
    One of the condition's characteristics is that, once affected by the disease, brain cells attempt to divide—possibly in order to balance out the death of other neurons—only to die, anyway.
    In any case, the further division of fully formed brain cells is unusual and does not happen in a healthy brain. The affected neurons' attempt at division is called the "cell cycle re-entry process."
    "It's been estimated that as much as 90% of neuron death that occurs in the Alzheimer's brain follows this cell cycle re-entry process, which is an abnormal attempt to divide," explains Professor Bloom.
    "By the end of the course of the disease, the patient will have lost about 30% of the neurons in the frontal lobes of the brain," he estimates.
    Study coauthor Erin Kodis—Professor Bloom's former doctoral student—formed her own hypothesis about what triggers this mechanism.

    Excess calcium, she believes, enters neurons through special receptors called NMDA receptors on the cells' surface. This drives brain cells to start dividing.

    Following a series of laboratory experiments, Kodis confirmed that her hypothesis was correct. This mechanism is set in motion before the formation of amyloid plaques, which are characteristic of Alzheimer's disease, in the brain.
    Eventually, however, molecules of an amino acid called beta amyloid stick together to form toxic amyloid plaques.

    Memantine may have 'potent properties'

    Kodis saw that when neurons encounter beta amyloid molecules in the early stages that precede plaque buildup, NMDA receptors open to receive the excess calcium that ultimately leads to their destruction.
    But then the researcher made another discovery: the drug memantine prevented cell cycle re-entry by closing the NMDA receptors on the surface of neurons.
    "The experiments suggest that memantine might have potent disease-modifying properties if it could be administered to patients long before they have become symptomatic and diagnosed with Alzheimer's disease."
    –Professor George Bloom
    "Perhaps this could prevent the disease or slow its progression long enough that the average age of symptom onset could be significantly later, if it happens at all," Professor Bloom adds.
    These findings are particularly promising; memantine has few known side effects, and those that have been reported are rare and do not have a major impact on an individual's well-being.
    Bloom believes that, in the future, a useful preventive approach might be to screen people for telling signs that they are exposed to Alzheimer's as early as possible.
    Specialists could then prescribe memantine to those at an increased risk of the disease, he says. People may have to take the drug throughout their lives to keep Alzheimer's at bay—or at least in check.
    "I don't want to raise false hopes," says Professor Bloom. However, he continues, "[I]f this idea of using memantine as a prophylactic pans out, it will be because we now understand that calcium is one of the agents that gets the disease started, and we may be able to stop or slow the process if done very early."
    Currently, Bloom and colleagues are planning a clinical trial to test the preventive strategy that they outlined in the study.
    To read more, click here

    Saturday, July 22, 2017

    Alzheimer’s Drug May Help Treat Traumatic Brain Injury

    9 posts going back to 2014 show memantine being useful for stroke recovery. And  yet I see nothing in the ASA, NSA or WSO about this or any reference to a memantine protocol anywhere. Once again proving we have NO stroke leadership and NO stroke strategy. Obviously, nobody cares. Your doctor doesn't care. Your stroke hospital doesn't care. You're screwed along with your children and grandchildren. Hopefully comeuppance hits the appropriate people. 

    Alzheimer’s Drug May Help Treat Traumatic Brain Injury


    Traumatic brain injury (TBI) is a major cause of disability and death globally, but medications have generally failed to benefit patients. A new study found that memantine, a drug that is used to treat dementia associated with Alzheimer's disease, may be a promising therapy.

    The study examined the effect of memantine on blood levels of neuron-specific enolase (NSE), a marker of neuronal damage, and the Glasgow Coma Scale (GCS) in patients with moderate TBI. The GCS is the most common scoring system used to describe the level of consciousness in a person following a TBI.
    Patients with moderate TBI who received memantine had significantly reduced blood levels of NSE by day 7 and marked improvements in their GCS scores on day 3 of the study.
    The study is published in The Journal of Clinical Pharmacology.
    Access the Paper:
    http://onlinelibrary.wiley.com/doi/10.1002/jcph.980/full

    Wednesday, November 25, 2015

    Memantine may not be covered through Medicare Part D

    From alz.org;

    Memantine coverage

    Memantine, which recently became available as a generic drug, may not be covered through Medicare Part D. If you or someone you know is taking memantine, check with your plan to inquire about coverage, or contact your State Health Insurance Program (SHIP) through Medicare and ask to speak to a counselor. You may also want to talk to your doctor regarding your options.


    You probably don't have to worry about this because I'm 100% positive that the research from July 2015 suggesting possible use for stroke has never been followed up on. I blame our fucking failures of stroke associations for that.

    Study of the neuroprotective effects of memantine in patients with mild to moderate ischemic stroke  July 2015

    Our results reveal that memantine added to standard treatment of CTEE(cerebral thromboembolic event) could result in a remarkable decrease in the NIHSS confirming improvement of the neurological function of the patients. 

    Sunday, October 25, 2015

    Antidepressants and Alzheimer’s Disease Drugs Might Boost Recovery in Stroke Patients

    So they are calling for more research. WHOM the fuck is going to answer that call and actually do some work? The stroke associations? Don't make me puke, they will never do anything so difficult as solving a clinical research problem, even if that problem is extensively defined for them and all they have to do is hire researchers to find the answer. You as a stroke survivor are screwed, there is no one in the world working to help you and future survivors get better.

    Antidepressants and Alzheimer’s Disease Drugs Might Boost Recovery in Stroke Patients

    But more research needed before recommending their routine use

    Released: 21-Oct-2015 6:05 PM EDT
    Source Newsroom: Loyola University Health System
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    Citations Drugs and Aging
    Newswise — MAYWOOD, Ill. – Evidence is mounting that drugs used to treat depression and Alzheimer’s disease also can help patients recover from strokes.But there are conflicting findings from studies of these and other drugs given to recovering stroke patients. Large, well-designed studies are needed before any drug can be recommended routinely for stroke recovery, according to a study in the journal Drugs and Aging by neurologists Xabier Beristain, MD, and Esteban Golombievski, MD, of Loyola University Medical Center and Loyola University Chicago Stritch School of Medicine.
    “These medications have not yet been clearly proven to be of benefit to patients recovering from strokes,” Dr. Beristain said. Speech and physical therapies traditionally have been the mainstays of stroke rehabilitation programs. But more than half of stroke survivors are left with some neurological impairment. “The limitations of these rehabilitation efforts have sparked an interest in finding other ways to enhance neurological recovery,” Drs. Beristain and Golombievski write.
    So far, the most promising drug treatments are antidepressants to improve motor recovery and Alzheimer’s disease drugs to boost recovery from aphasia (impaired ability to speak, write and understand verbal and written language).
    About one in three stroke patients suffers depression, which can limit a patient’s ability to participate in rehabilitation. There is mounting evidence that the class of antidepressants known as selective serotonin reuptake inhibitors, or SSRIs (such as Prozac, Paxil and Celexa), may enhance neurological recovery beyond their effect on mood. Another type of antidepressant, norepinephrine reuptake inhibitor (NRI) also has shown benefit.
    An analysis of 56 clinical trials of SSRIs found the drugs appeared to improve dependence, disability, neurological impairment, anxiety and depression after stroke. However, these findings should be taken with caution because the studies have different designs. Several additional clinical trials now underway are evaluating the use of antidepressants to enhance stroke recovery.
    There is growing evidence that Alzheimer’s disease drugs called acetylcholinesterase inhibitors (including Aricept, Exelon and Razadyne) can improve aphasia in stroke patients. A second type of Alzheimer’s medication under study is memantine (Namenda). When used in combination with therapy, memantine has shown language benefits lasting at least one year when compared with a placebo. But clinical evidence of memantine for stroke recovery remains limited.
    So far, most studies of these and other drugs used for stroke recovery have been small, employing different methodologies and time windows between the stroke and the clinical intervention.
    We need well-designed, large clinical trials with enough power to establish the usefulness of medications as adjuvants to rehabilitation before we can routinely recommend the use of these agents to enhance neurological recovery after stroke,” Drs. Beristain and Golombievski write.
    Dr. Beristain is an associate professor in the Department of Neurology of Loyola University Chicago Stritch School of Medicine. Dr. Golombievski is a former neurology fellow at Loyola.
    The paper is titled “Pharmacotherapy to Enhance Cognitive and Motor Recovery Following Stroke.”

    Thursday, July 30, 2015

    Study of the neuroprotective effects of memantine in patients with mild to moderate ischemic stroke

    I bet memantine is not being agressively followed up to create a translational stroke protocol for its use. I'll bet 50 years before it gets used, allowing trillions of neurons to die in the meantime. How can the ASA, NSA and WSO live with themselves for allowing such needless neuron deaths to occur?
    http://www.ncbi.nlm.nih.gov/pubmed/25237355

    Abstract

    Ischemic stroke is amongst the top four causes of mortality and the leading cause of disability in the world. The aim of this study was to evaluate the efficacy of a high dose memantine on neurological function of patients with ischemic stroke. In a randomized, 2 armed, open-label study, patients with mild to moderate cerebral thromboembolic event (CTEE) who admitted to Imam Hossein Hospital, Tehran, Iran, during preceding 24 hours, entered the study. Patients allocated in two study groups of memantine (as add-on therapy) and control. All patients were managed based on the American Heart Association and American Stroke Association (AHA/ASA) guidelines. Patients in memantine group received conventional treatment plus memantine 20 mg TID. The National Institute of Health Stroke Scale (NIHSS) was determined and recorded daily. The primary objective was comparison of the changes in NIHSS in the study groups at day 1 and day 5 of intervention. Significance level of p<0.05 was considered for statistical analysis. Patients were randomly allocated in control (15 women and 14 men, age 70.78 ± 10.92 years) and memantine (16 women and 8 men, age 73.33 ± 9.35 years) groups. There were no significant differences in age and sex distribution of two study groups as well as in comorbidities and concurrent drugs. NIHSS changes were significantly different between control (1.24 ± 0.96) and memantine group (2.96 ± 0.1), (p < 0.0001). Our results reveal that memantine added to standard treatment of CTEE could result in a remarkable decrease in the NIHSS confirming improvement of the neurological function of the patients.

    The dichotomy of memantine treatment for ischemic stroke: dose-dependent protective and detrimental effects

    You're going to have to know when you are having your stroke so you can get proper pretreatment. Good luck with that.
    http://www.ncbi.nlm.nih.gov/pubmed/25407270

    Abstract

    Excitotoxicity is a major contributor to cell death during the acute phase of ischemic stroke but aggressive pharmacological targeting of excitotoxicity has failed clinically. Here we investigated whether pretreatment with low doses of memantine, within the range currently used and well tolerated for the treatment of Alzheimer's disease, produce a protective effect in stroke. A coculture preparation exposed to modeled ischemia showed cell death associated with rapid glutamate rises and cytotoxic Ca(2+) influx. Cell death was significantly enhanced in the presence of high memantine concentrations. However, low memantine concentrations significantly protected neurons and glia via excitotoxic cascade interruption. Mice were systemically administered a range of memantine doses (0.02, 0.2, 2, 10, and 20 mg/kg/day) starting 24 hours before 60 minutes reversible focal cerebral ischemia and continuing for a 48-hour recovery period. Low dose (0.2 mg/kg/day) memantine treatment significantly reduced lesion volume (by 30% to 50%) and improved behavioral outcomes in stroke lesions that had been separated into either small/striatal or large/striatocortical infarcts. However, higher doses of memantine (20 mg/kg/day) significantly increased injury. These results show that clinically established low doses of memantine should be considered for patients 'at risk' of stroke, while higher doses are contraindicated.

    Memantine enhances recovery from stroke

    Whom is following up on this? Who has updated the stroke strategy? Who has the stroke strategy? I somehow missed this when it came out a year ago.
    http://www.ncbi.nlm.nih.gov/pubmed/24938836

    Erratum in

    • Stroke. 2014 Nov;45(11):e238.

    Abstract

    BACKGROUND AND PURPOSE:

    Stroke treatment is constrained by limited treatment windows and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable poststroke plasticity, which could allow treatment with recovery-modulating agents. Memantine is a well-tolerated N-methyl-D-aspartate glutamate receptor antagonist in common use for Alzheimer disease.

    METHODS:

    Memantine, 30 mg/kg per day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke.

    RESULTS:

    Although there was no difference in infarct size, behavior, or optical intrinsic signal maps in the first 7 days after stroke, mice treated chronically with memantine showed significant improvements in motor control, measured by cylinder test and grid-walking performance, compared with vehicle-treated animals. Optical intrinsic signal revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor and phosphorylated-tropomyosin-related kinase-B receptor expression.

    CONCLUSIONS:

    Our results suggest that memantine improves stroke outcomes in an apparently non-neuroprotective manner involving increased brain-derived neurotrophic factor signaling, reduced reactive astrogliosis, and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of memantine make it an attractive candidate for clinical translation.

    Monday, June 23, 2014

    Memantine Enhances Recovery From Stroke

    And why the f*ck won't your doctor try this after your stroke? I bet any patient would agree to signing the release form. If my doctor had any brains at all he could have asked me to allow immediate administration of statins even though testing had only been proven in rats 3 years prior.
    If you want something like this you are going to have to scream at your doctors because they will never try something new that might save a whole slew of your neurons. And what the hell are you paying them for? To sit around and watch your neurons die in the neuronal cascade of death?
    http://stroke.ahajournals.org/content/45/7/2093.abstract?etoc
    1. Correspondence to Kevin C. Brennan, MD, 383 Colorow Dr, Room 364, Salt Lake City, UT 84103. E-mail k.c.brennan@hsc.utah.edu.
    1. * Drs López-Valdés and Clarkson contributed equally.

    Abstract

    Background and Purpose—Stroke treatment is constrained by limited treatment windows and the clinical inefficacy of agents that showed preclinical promise. Yet animal and clinical data suggest considerable poststroke plasticity, which could allow treatment with recovery-modulating agents. Memantine is a well-tolerated N-methyl-D-aspartate glutamate receptor antagonist in common use for Alzheimer disease.
    Methods—Memantine, 30 mg/kg per day, or vehicle, was delivered chronically in drinking water beginning >2 hours after photothrombotic stroke.
    Results—Although there was no difference in infarct size, behavior, or optical intrinsic signal maps in the first 7 days after stroke, mice treated chronically with memantine showed significant improvements in motor control, measured by cylinder test and grid-walking performance, compared with vehicle-treated animals. Optical intrinsic signal revealed an increased area of forepaw sensory maps at 28 days after stroke. There was decreased reactive astrogliosis and increased vascular density around the infarcted cortex. Peri-infarct Western blots revealed increased brain-derived neurotrophic factor and phosphorylated-tropomyosin–related kinase-B receptor expression.
    Conclusions—Our results suggest that memantine improves stroke outcomes in an apparently non-neuroprotective manner involving increased brain-derived neurotrophic factor signaling, reduced reactive astrogliosis, and improved vascularization, associated with improved recovery of sensory and motor cortical function. The clinical availability and tolerability of memantine make it an attractive candidate for clinical translation.

    Tuesday, January 28, 2014

    Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial

    Prevention would probably be better.

    This is what I'm doing for prevention.
    This is what the Harvard Medical School suggests.
    Generic dementia prevention here
    Alpha tocopherol is not standard vitamin E. You know the drill, ask your doctor. 

    The latest here: 

    Effect of vitamin E and memantine on functional decline in Alzheimer disease: the TEAM-AD VA cooperative randomized trial


    Author information

    • 1Minneapolis VA Health Care System, Minneapolis, Minnesota.
    • 2James J. Peters VA Medical Research Center, New York, New York.
    • 3William S. Middleton Memorial Veterans Hospital, Madison, Wisconsin.
    • 4Cooperative Studies Program Clinical Research Pharmacy Coordinating Center, Albuquerque, New Mexico.
    • 5Louis Stokes Cleveland VA Medical Center, Cleveland, Ohio6Case Western Reserve University School of Medicine, Cleveland, Ohio.
    • 6Washington DC VA Medical Center, Washington, DC.
    • 7University of Pennsylvania School of Medicine, Philadelphia.
    • 8Miami VA Healthcare System, Miami, Florida.
    • 9VA Maryland Healthcare System, Baltimore11University of Maryland Medical School, Department of Psychiatry, Baltimore.
    • 10VA North Texas Health Care System, Dallas.
    • 11Ralph H. Johnson VA Medical Center, Charleston, South Carolina14Department of Health Studies, Medical University of South Carolina, Charleston15Roper St Francis Healthcare, Charleston, South Carolina.
    • 12VA Ann Arbor Healthcare System, Ann Arbor, Michigan.
    • 13VA Caribbean Healthcare System, San Juan, Puerto Rico.
    • 14Bay Pines VA Healthcare System, Bay Pines, Florida.
    • 15VA Boston Healthcare System, Boston, Massachusetts.
    • 16VA Puget Sound Health Care System, Seattle, Washington21Department of Psychiatry and Behavioral Sciences, University of Washington, Seattle.
    • 17Iowa City VA Medical Center, Iowa City, Iowa23University of Iowa, Iowa City.
    • 18W. G. (Bill) Hefner VA Medical Center, Salisbury, North Carolina.
    • 19Cooperative Studies Program Coordinating Center, VA Connecticut Healthcare System, West Haven26Yale University School of Public Health, New Haven, Connecticut.

    Abstract

    IMPORTANCE:

    Although vitamin E and memantine have been shown to have beneficial effects in moderately severe Alzheimer disease (AD), evidence is limited in mild to moderate AD.

    OBJECTIVE:

    To determine if vitamin E (alpha tocopherol), memantine, or both slow progression of mild to moderate AD in patients taking an acetylcholinesterase inhibitor.

    DESIGN, SETTING, AND PARTICIPANTS:

    Double-blind, placebo-controlled, parallel-group, randomized clinical trial involving 613 patients with mild to moderate AD initiated in August 2007 and concluded in September 2012 at 14 Veterans Affairs medical centers.

    INTERVENTIONS:

    Participants received either 2000 IU/d of alpha tocopherol (n = 152), 20 mg/d of memantine (n = 155), the combination (n = 154), or placebo (n = 152).

    MAIN OUTCOMES AND MEASURES:

    Alzheimer's Disease Cooperative Study/Activities of Daily Living (ADCS-ADL) Inventory score (range, 0-78). Secondary outcomes included cognitive, neuropsychiatric, functional, and caregiver measures.

    RESULTS:

    Data from 561 participants were analyzed (alpha tocopherol = 140, memantine = 142, combination = 139, placebo = 140), with 52 excluded because of a lack of any follow-up data. Over the mean (SD) follow-up of 2.27 (1.22) years, ADCS-ADL Inventory scores declined by 3.15 units (95% CI, 0.92 to 5.39; adjusted P = .03) less in the alpha tocopherol group compared with the placebo group. In the memantine group, these scores declined 1.98 units less (95% CI, -0.24 to 4.20; adjusted P = .40) than the placebo group's decline. This change in the alpha tocopherol group translates into a delay in clinical progression of 19% per year compared with placebo or a delay of approximately 6.2 months over the follow-up period. Caregiver time increased least in the alpha tocopherol group. All-cause mortality and safety analyses showed a difference only on the serious adverse event of "infections or infestations," with greater frequencies in the memantine (31 events in 23 participants) and combination groups (44 events in 31 participants) compared with placebo (13 events in 11 participants).

    CONCLUSIONS AND RELEVANCE:

    Among patients with mild to moderate AD, 2000 IU/d of alpha tocopherol compared with placebo resulted in slower functional decline. There were no significant differences in the groups receiving memantine alone or memantine plus alpha tocopherol. These findings suggest benefit of alpha tocopherol in mild to moderate AD by slowing functional decline and decreasing caregiver burden.

    TRIAL REGISTRATION:

    clinicaltrials.gov Identifier: NCT00235716.

    Sunday, December 16, 2012

    Study: Even the smallest stroke can damage brain tissue, impair cognitive function

    Who is going to take the lead in getting this into clinical trials? I don't have to worry about the ASA, NSA or WSO doing it because they have no intention  of working on specific tasks that might help survivors. That would require initiative. They have absolutely none.
     http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html
     Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience.  "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge.  "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp
    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp
    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp
    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp
    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp
    Blocking a single tiny blood vessel in the brain can harm neural tissue and even alter behavior, a new study from the University of California, San Diego has shown. But these consequences can be mitigated by a drug already in use, suggesting treatment that could slow the progress of dementia associated with cumulative damage to miniscule blood vessels that feed brain cells. The team reports their results in the December 16 advance online edition of Nature Neuroscience. Ads by Google Brain Training Games - Improve memory and attention with scientific brain games. Free Trial - www.lumosity.com "The brain is incredibly dense with vasculature. It was surprising that blocking one small vessel could have a discernable impact on the behavior of a rat," said Andy Y. Shih, lead author of the paper who completed this work as a postdoctoral fellow in physics at UC San Diego. Shih is now an assistant professor at the Medical University of South Carolina. Working with rats, Shih and colleagues used laser light to clot blood at precise points within small blood vessels that dive from the surface of the brain to penetrate neural tissue. When they looked at the brains up to a week later, they saw tiny holes reminiscent of the widespread damage often seen when the brains of patients with dementia are examined as a part of an autopsy. These micro-lesions are too small to be detected with conventional MRI scans, which have a resolution of about a millimeter. Nearly two dozen of these small vessels enter the brain from a square millimeter area of the surface of the brain. "It's controversial whether that sort of damage has consequences, although the tide of evidence has been growing as human diagnostics improve," said David Kleinfeld, professor of physics and neurobiology, who leads the research group. To see whether such minute damage could change behavior, the scientists trained thirsty rats to leap from one platform to another in the dark to get water. The rats readily jump if they can reach the second platform with a paw or their snout, or stretch farther to touch it with their whiskers. Many rats can be trained to rely on a single whisker if the others are clipped, but if they can't feel the far platform, they won't budge. Ads by Google Brain Exercises Games - Fun Games to Chisel Your Brain Download Tons of Them for Free! - www.APlusGamer.com 3 Early Signs of Dementia - Doctor: Know These 3 Warning Signs You're About to Suffer Dementia - www.newsmax.com "The whiskers line up in rows and each one is linked to a specific spot in the brain," Shih said. "By training them to use just one whisker, we were able to distill a behavior down to a very small part of the brain." When Shih blocked single microvessels feeding a column of brain cells that respond to signals from the remaining whisker, the rats still crossed to the far platform when the gap was small. But when it widened beyond the reach of their snouts, they quit. The FDA-approved drug memantine, prescribed to slow one aspect of memory decline associated with Alzheimer's disease, ameliorated these effects. Rats that received the drug jumped whisker-wide gaps, and their brains showed fewer signs of damage. "This data shows us, for the first time, that even a tiny stroke can lead to disability," said Patrick D. Lyden, a co-author of the study and chair of the department of neurology at Cedars-Sinai Medical Center in Los Angeles. "I am afraid that tiny strokes in our patients contribute—over the long term—to illness such as dementia and Alzheimer's disease," he said, adding that "better tools will be required to tell whether human patients suffer memory effects from the smallest strokes." "We used powerful tools from biological physics, many developed in Kleinfeld's laboratory at UC San Diego, to link stroke to dementia on the unprecedented small scale of single vessels and cells," Shih said. "At my new position at MUSC, I plan to work on ways to improve the detection of micro-lesions in human patients with MRI. This way clinicians may be able to diagnose and treat dementia earlier." —Susan Brown

    Read more at: http://medicalxpress.com/news/2012-12-smallest-brain-tissue-impair-cognitive.html#jCp