Long-term prediction of functional outcome after stroke using single items of the Barthel Index at discharge from rehabilitation centre

This is stupid, using a secondary measure to predict outcomes. You should be using something objective like how large and where is the dead area.
http://informahealthcare.com/doi/abs/10.3109/09638288.2013.793411

Abstract

Purpose: To determine the prognostic value of single items of the Barthel Index (BI) at discharge from rehabilitation, in predicting independence in personal activities of daily living (ADL) (BI score ≥95/100) at five years after stroke. Method: People with stroke were recruited consecutively from four European rehabilitation centres. BI was assessed on discharge and at five years after stroke. Stepwise multivariate logistic regression analysis was used to determine independent predictors of BI score ≥95/100 at five years after stroke. Thereupon, percentage chance of reaching BI ≥ 95/100 at five years after stroke was calculated. Results: Data were available for 153 patients. Independence in dressing (odds ratio (OR) = 5.22, 95% confidence interval (CI) = 1.85–14.76, p = 0.002) and bathing (OR = 8.10, 95% CI = 3.40–19.32, p  < 0.0001) were independent predictors. Independence in both items resulted in 74.1% (57.6–85.8) chance of reaching BI ≥ 95/100 at five years after stroke. Dependence in both items resulted in 6.3% (5.1–7.9) chance. Independence in bathing, but dependence in dressing resulted in 35.4% (30.7–40.4) chance whereas the opposite resulted in 26.1% (20.7–32.3) chance. Conclusion: Simple assessment of dressing and bathing on discharge from rehabilitation enables therapeutic staff to predict prognosis for long-term independence in personal ADL. This method can be used for early identification of persons with stroke who need intensive follow-up.Implications for Rehabilitation

• (In)dependence for dressing and bathing at discharge from a rehabilitation centre are significant factors in the prediction of (in)dependence in personal ADL at five years after stroke.
• This predictive tool can be used for targeting inpatient stroke rehabilitation and early identification of those patients who need intensive follow-up.

Read More: http://informahealthcare.com/doi/abs/10.3109/09638288.2013.793411

Interaction and Antagonistic Roles of NF-kappaB and Hes6 in the Regulation of Cortical Neurogenesis

I have no clue what this means and no understanding of what cortical progenitor cells are. Doctor question it is.
 http://mcb.asm.org/content/early/2013/05/15/MCB.01610-12.abstract

ABSTRACT

The involvement of nuclear factor-kappaB (NF-κB) in several processes in the postnatal and adult brain, ranging from neuronal survival to synaptogenesis and plasticity, has been documented. In contrast, little is known about the functions of NF-κB during embryonic brain development. It is shown here that NF-κB is selectively activated in neocortical neural progenitor cells in the developing mouse telencephalon. Blockade of NF-κB activity leads to premature cortical neuronal differentiation and depletion of the progenitor cell pool. Conversely, NF-κB activation causes decreased cortical neurogenesis and expansion of the progenitor cell compartment. This effect is antagonized by the pro-neuronal transcription factor Hes6, which physically and functionally interacts with RelA-containing NF-κB complexes in cortical progenitor cells. In turn, NF-κB exerts an inhibitory effect on the ability of Hes6 to promote cortical neuronal differentiation. These results reveal previously uncharacterized functions, and modes of regulation, for NF-κB and Hes6 during cortical neurogenesis.

Role of HIF-1α-activated Epac1 on HSC-mediated neuroplasticity in stroke model

I have no clue what this means and no understanding of what an ischemic muscle is. Doctor question it is.
http://www.sciencedirect.com/science/article/pii/S0969996113001484

Abstract

Exchange protein activated by cAMP-1 (Epac1) plays an important role in cell proliferation, cell survival and neuronal signaling, and activation of Epac1 in endothelial progenitor cells increases their homing to ischemic muscles and promotes neovascularization in a model of hind limb ischemia. Moreover, upregulation of Epac1 occurs during organ development and in diseases such as myocardial hypertrophy, diabetes, and Alzheimer's disease. We report here that hypoxia upregulated Epac1 through HIF-1α induction in the CD34-immunosorted human umbilical cord blood hematopoietic stem cells (hUCB³⁴). Importantly, implantation of hUCB³⁴ subjected to hypoxia-preconditioning (HP-hUCB³⁴) improved stroke outcome, more than did implantation of untreated hUCB³⁴, in rodents subjected to cerebral ischemia, and this required Epac1-to-matrix metalloprotease (MMP) signaling. This improved therapeutic efficacy correlated with better engraftment and differentiation of these cells in the ischemic host brain. In addition, more than did implantation of untreated HP-hUCB³⁴, implantation of HP-hUCB³⁴ improved cerebral blood flow into the ischemic brain via induction of angiogenesis, facilitated proliferation/recruitment of endogenous neural progenitor cells in the ischemic brain, and promoted neurite outgrowth following cerebral ischemia. Consistent with our proposed role of Epac1-to-MMP signaling in hypoxia-preconditioning, the above mentioned effects of implanting HP-hUCB³⁴ could be abolished by pharmacological inhibition and genetic disruption/deletion of Epac1 or MMPs. We have discovered a HIF-1α-to-Epac1-to-MMP signaling pathway that is required for the improved therapeutic efficacy resulting from hypoxia preconditioning of hUCB³⁴ in vitro prior to their implantation into the host brain in vivo.

First drug to improve heart failure mortality in over a decade

You will want to read this if you are taking statins. Your doctor should know about this side effect of statins.
http://www.alphagalileo.org/ViewItem.aspx?ItemId=131385&CultureCode=en
Coenzyme Q10 decreases all cause mortality by half, according to the results of a multicentre randomised double blind trial presented today at Heart Failure 2013 congress. It is the first drug to improve heart failure mortality in over a decade and should be added to standard treatment, according to lead author Professor Svend Aage Mortensen (Copenhagen, Denmark).
Heart Failure 2013 is being held from 25-28 May in Lisbon, Portugal. It is the main annual meeting of the Heart Failure Association of the European Society of Cardiology (1).
Coenzyme Q10 (CoQ10) occurs naturally in the body and is essential to survival. CoQ10 works as an electron carrier in the mitochondria, the powerhouse of the cells, to produce energy and is also a powerful antioxidant. It is the only antioxidant that humans synthesise in the body.
CoQ10 levels are decreased in the heart muscle of patients with heart failure, with the deficiency becoming more pronounced as heart failure severity worsens. Statins are used to treat many patients with heart failure because they block the synthesis of cholesterol, but these drugs also block the synthesis of CoQ10, which further decreases levels in the body.
Double blind controlled trials have shown that CoQ10 improves symptoms, functional capacity and quality of life in patients with heart failure with no side effects. But until now, no trials have been statistically powered to address effects on survival.

More at link.

Gamma Aminobutyric Acid Receptor Agonists for Acute Stroke

Now if we just had some doctors with initiative, we could be trying out this along with my earlier 165 hyperacute options and actually save trillions of neurons from dying. Or just a very loud mouth type A personality that won't take doing nothing for an answer. I bet it will be the type A personality that advances stroke rehab rather than any doctor, but I'm willing to be proven wrong.
http://stroke.ahajournals.org/content/44/6/e65

Introduction

Gamma aminobutyric acid (GABA) receptor agonists have shown to be effective in reducing infarct size and improving functional outcome in animal models of cerebral ischemia. However, the sedation effects of GABA receptor agonists limited the application in acute stroke patients because of the potential risk of stupor.

Materials and Methods

Objective

The aim of this study is to determine the efficacy and safety of GABA receptor agonists in the treatment of acute stroke.

Types of Studies

Randomized controlled trials.

Types of Participants

Acute stroke patients within 12 hours after stroke onset.

Types of Interventions

GABA receptor agonists in comparison with placebo.

Primary Outcomes

Death or dependency, defined as a Barthel Index score of ≤60, or the modified Rankin Scale graded 3 to 5, and adverse events.

Secondary Outcomes

Functional independence, defined as Barthel Index score >60, or modified Rankin Scale <3, and neurological function measured by other stroke scales.

Results

We included 5 trials with 3838 randomized patients. The methodological quality of the included trials was generally good, with low risk of bias. Four trials measured death and dependency at 3 months in chlormethiazole versus placebo without significant difference (2909 patients; risk ratio [RR], 1.03, 95% confidence interval [CI], 0.95–1.11). One trial measured this outcome between diazepam and placebo (849 patients; RR, 0.94; 95% CI, 0.82–1.07). In the subgroup analysis of total anterior circulation syndrome, a higher percentage of functional independence was found in the chlormethiazole group (635 patients; RR, 1.33; 95% CI, 1.09–1.64). The frequent adverse events related to chlormethiazole were somnolence (2527 patients; RR, 4.56, 95% CI, 3.50–5.95) and rhinitis (2527 patients; RR, 4.75, 95% CI

Tim Curry’s Stroke Major, But’s He’s Recovering at Home; Can Speak, Might Sing

I'll only point out 1 bone of contention.
http://www.denofgeek.us/movies/tim-curry/121986/tim-curry%E2%80%99s-stroke-major-but%E2%80%99s-he%E2%80%99s-recovering-at-home-can-speak-might-sing
According to published reports, Tim Curry is recovering after suffering a major stroke last night. Curry’s agent said he’s back at home recovering and, contrary to earlier reports, he has not lost his ability to speak.
Tim Curry’s stroke happened last night at his LA home. Sources say Tim Curry’s stroke was a major one, but he is expected to recover fully. Marcia Hurwitz, Tim Curry’s long-time agent, told the press that "Tim is doing great. He absolutely can speak and is recovering at this time and in great humor."

Whomever is saying fully recover has no clue what they are talking about. Nobody is doing any kind of damage diagnosis today and there is no understanding of what damage continues to occur during the first week due to the neuronal cascade of death. Unless it was not major and was only a TIA.

Dopamine restores reward prediction errors in old age

From my reading of this our doctors should be concerned and be using a protocol that restores dopamine prior to getting our regular therapy.
http://www.nature.com/neuro/journal/v16/n5/full/nn.3364.html

Abstract

Senescence affects the ability to utilize information about the likelihood of rewards for optimal decision-making. Using functional magnetic resonance imaging in humans, we found that healthy older adults had an abnormal signature of expected value, resulting in an incomplete reward prediction error (RPE) signal in the nucleus accumbens, a brain region that receives rich input projections from substantia nigra/ventral tegmental area (SN/VTA) dopaminergic neurons. Structural connectivity between SN/VTA and striatum, measured by diffusion tensor imaging, was tightly coupled to inter-individual differences in the expression of this expected reward value signal. The dopamine precursor levodopa (L-DOPA) increased the task-based learning rate and task performance in some older adults to the level of young adults. This drug effect was linked to restoration of a canonical neural RPE. Our results identify a neurochemical signature underlying abnormal reward processing in older adults and indicate that this can be modulated by L-DOPA

Virtual Walking Training Program Using a Real-world Video Recording for Patients with Chronic Stroke: A Pilot Study

You will need to have your doctor or therapist translate what a real-world video recording is. I'm stupid that way.
http://www.hubmed.org/display.cgi?uids=23598900&
The purpose of this study was to investigate the effectiveness of the virtual walking training program using a real-world video recording on walking balance and spatiotemporal gait parameters in patients with chronic stroke.Fourteen patients with chronic stroke were randomly assigned to either the experimental group (n = 7) or the control group (n = 7). The subjects in both groups underwent a standard rehabilitation program; in addition, the experimental group participated in the virtual walking training program using a real-world video recording for 30 mins a day, three times a week, for 6 wks, and the control group participated in treadmill gait training for 30 mins a day, three times a week, for 6 wks. Walking balance was measured using the Berg Balance Scale (BBS) and the Timed Up and Go test. Gait performance was measured using an electrical walkway system.In walking balance, greater improvement on the Berg Balance Scale (experimental group: 4.14 vs. control group: 1.85) and the Timed Up and Go test (-2.25 vs. -0.94) was observed in the experimental group compared with the control group (P < 0.05). In the spatiotemporal gait parameters, greater improvement on velocity (25.40 vs. 9.74) and cadence (26.71 vs. 11.11) was observed in the experimental group compared with the control group (P < 0.05).This study demonstrated the positive effects of the virtual walking training program using a real-world video recording on gait performance. These findings suggest that the virtual walking training program using a real-world video recording may be a valid approach to enhance gait performance in patients with chronic stroke.

Blood-Brain Barrier Integrity Suffers Days After Ischemic Stroke Leading To Serious Complications

I wish they would at least compare and contrast their findings to the earlier one here:  from January 2013.
Kruppel-like Factor 2 Protects Against Ischemic Stroke by Regulating Endothelial Blood Brain Barrier Function
the new one here;
http://www.medicalnewstoday.com/releases/260812.php 
 
While the effects of acute stroke have been widely studied, brain damage during the subacute phase of stroke has been a neglected area of research. Now, a new study by the University of South Florida reports that within a week of a stroke caused by a blood clot in one side of the brain, the opposite side of the brain shows signs of microvascular injury.

Stroke is a leading cause of death and disability in the United States, and increases the risk for dementia.

"Approximately 80 percent of strokes are ischemic strokes, in which the blood supply to the brain is restricted, causing a shortage of oxygen," said study lead author Svitlana Garbuzova-Davis, PhD, associate professor in the USF Department of Neurosurgery and Brain Repair. "Minutes after ischemic stroke, there are serious effects within the brain at both the molecular and cellular levels. One understudied aspect has been the effect of ischemic stroke on the competence of the blood-brain barrier and subsequent related events in remote brain areas."

Using a rat model, researchers at USF Health investigated the subacute phase of ischemic stroke and found deficits in the microvascular integrity in the brain hemisphere opposite to where the initial stroke injury occured.

The study was published in the journal PLOS One.

The USF team found that "diachisis," a term used to describe certain brain deficits remote from primary insult, can occur during the subacute phase of ischemic stroke. The research discovered diachisis is closely related to a breakdown of the blood-brain barrier, which separates circulating blood from brain tissue.

In the subacute phase of an ischemic stroke, when the stroke-induced disturbances in the brain occur in remote brain microvessels, several areas of the brain are affected by a variety of injuries, including neuronal swelling and diminished myelin in brain structures. The researchers suggest that recognizing the significance of microvascular damage could make the blood-brain barrier (BBB) a therapeutic "target" for future neuroprotective strategies for stroke patients.

The mechanisms of BBB permeability at different phases of stroke are poorly understood. While there have been investigations of BBB integrity and processes in ischemic stroke, the researchers said, most examinations have been limited to the phase immediately after stroke, known as acute stroke. Their interest was in determining microvascular integrity in the brain hemisphere opposite to an initial stroke injury at the subacute phase.

Accordingly, this study using rats with surgically-simulated strokes was designed to investigate the effect of ischemic stroke on the BBB in the subacute phase, and the effects of a compromised BBB upon various brain regions, some distant from the stroke site.

"The aim of this study was to characterize subacute diachisis in rats modeled with ischemic stroke," said co-author Cesar Borlongan, PhD, professor and vice chairman for research in the Department of Neurosurgery and Brain Repair and director of the USF Center for Aging and Brain Repair. "Our specific focus was on analyzing the condition of the BBB and the processes in the areas of the brain not directly affected by ischemia. BBB competence in subacute diachisis is uncertain and needed to be studied."

Their findings suggest that damage to the BBB, and subsequent vascular leakage as the BBB becomes more permeable, plays a major role in subacute diachisis.

The increasing BBB permeability hours after the simulated stroke, and finding that the BBB "remained open" seven days post-stroke, were significant findings, said Dr. Garbuzova-Davis, who is also a researcher in USF Center for Aging and Brain Repair. "Since increased BBB permeability is often associated with brain swelling, BBB leakage may be a serious and life-threatening complication of ischemic stroke."

Another significant aspect was the finding that autophagy -- a mechanism involving cell degradation of unnecessary or dysfunctional cellular components --plays a role in the subacute phase of ischemia. Study results showed that accumulation of numerous autophagosomes within endothelial cells in microvessels of both initially damaged and non-injured brain areas might be closely associated with BBB damage.

Autophagy is a complex but normal process usually aimed at "self-removing" damaged cell components to promote cell survival. It was unclear, however, whether the role of autophagy in subacute post-ischemia was promoting cell survival or cell death.

More than 30 percent of patients who survive strokes develop dementia within two years, the researchers noted.

"Although dementia is complex, vascular damage in post-stroke patients is a significant risk factor, depending on the severity, volume and site of the stroke," said study co-author Dr. Paul Sanberg, USF senior vice president for research and innovation. "Ischemic stroke might initiate neurodegenerative dementia, particularly in the aging population."

The researchers conclude that repair of the BBB following ischemic stroke could potentially prevent further degradation of surviving neurons.

"Recognizing that the BBB is a therapeutic target is important for developing neuroprotective strategies," they said

Regenerating spinal cord fibers may be treatment for stroke-related disabilities

Don't expect any followup from any stroke association, that would involve real work.
http://medicalxpress.com/news/2013-05-regenerating-spinal-cord-fibers-treatment.html
A study by researchers at Henry Ford Hospital found "substantial evidence" that a regenerative process involving damaged nerve fibers in the spinal cord could hold the key to better functional recovery by most stroke victims.

The findings may offer new hope to those who suffer stroke, the leading cause of long-term disability in adults. Although most stroke victims recover some ability to voluntarily use their hands and other body parts, about half are left with weakness on one side of their bodies, while a substantial number are permanently disabled. The study is published in the current issue of Stroke and is available online. Discovering a treatment to improve or restore this lost motor function in stroke patients is a holy grail for neurologists, because none exists, primarily due to unsolved mysteries about how the brain and nerves repair themselves. The new Henry Ford research was intended to solve some of those mysteries. It focused on changes in axons – the fibers, the nerve signal "transmission" lines within the spinal cord that affect voluntary movement after stroke.

Read more at: http://medicalxpress.com/news/2013-05-regenerating-spinal-cord-fibers-treatment.html#jCp

 The findings may offer new hope to those who suffer stroke, the leading cause of long-term disability in adults. Although most stroke victims recover some ability to voluntarily use their hands and other body parts, about half are left with weakness on one side of their bodies, while a substantial number are permanently disabled. The study is published in the current issue of Stroke and is available online. Discovering a treatment to improve or restore this lost motor function in stroke patients is a holy grail for neurologists, because none exists, primarily due to unsolved mysteries about how the brain and nerves repair themselves. The new Henry Ford research was intended to solve some of those mysteries. It focused on changes in axons – the fibers, the nerve signal "transmission" lines within the spinal cord that affect voluntary movement after stroke.
More at link or look up the study in Stroke magazine.

A study by researchers at Henry Ford Hospital found "substantial evidence" that a regenerative process involving damaged nerve fibers in the spinal cord could hold the key to better functional recovery by most stroke victims.

Read more at: http://medicalxpress.com/news/2013-05-regenerating-spinal-cord-fibers-treatment.html#jCp

A study by researchers at Henry Ford Hospital found "substantial evidence" that a regenerative process involving damaged nerve fibers in the spinal cord could hold the key to better functional recovery by most stroke victims.

Read more at: http://medicalxpress.com/news/2013-05-regenerating-spinal-cord-fibers-treatment.html#jCp

Low-intensity treadmill exercise and/or bright light promote neurogenesis in adult rat brain

What a simple research experiment on humans. Any clinic could do it. Why hasn't your doctor started this?  Neurogenesis after stroke should  be one of the protocol endpoints.
http://scholar.google.com/scholar_url?hl=en&q=http://www.sjzsyj.org:8080/Jweb_sjzs/CN/article/downloadArticleFile.do%3FattachType%3DPDF%26id%3D548&sa=X&scisig=AAGBfm2F-7v0mEI0P1Ye61vCozHBSGA_Ww&oi=scholaralrt
Abstract
The hippocampus is a brain region responsible for learning and memory functions. The purpose of this study was to investigate the effects of low-intensity exercise and bright light exposure on neurogenesis and brain-derived neurotrophic factor expression in adult rat hippocampus. Male Sprague-Dawley rats were randomly assigned to control, exercise, light, or exercise + light groups (n = 9 per group). The rats in the exercise group were subjected to treadmill exercise (5 days per week, 30 minutes per day, over a 4-week period), the light group rats were irradiated (5 days per week, 30 minutes per day, 10 000 lx, over a 4-week period), the exercise + light group rats were subjected to treadmill exercise in combination with bright light exposure, and the control group rats remained sedentary over a 4-week period. Compared with the control group, there was a significant increase in neurogenesis in the hippocampal dentate gyrus of rats in the exercise, light, and exercise + light groups. Moreover, the expression level of brain-derived neurotrophic factor in the rat hippocampal dentate gyrus was significantly higher in the exercise group and light group than that in the control group. Interestingly, there was no significant difference in brain-derived neurotrophic factor expression between the control group and exercise + light group. These results indicate that low-intensity treadmill exercise (first 5 minutes at a speed of 2 m/min, second 5 minutes at a speed of 5 m/min, and the last 20 minutes at a speed of 8 m/min) or bright-light exposure therapy induces positive biochemical changes in the brain. In view of these findings, we propose that moderate exercise or exposure to sunlight during childhood can be beneficial for neural development.

Can High-Dose Statins Improve Outcomes after Aneurysm-Related Stroke?

Well they are already proven to help after ischemic stroke. Be careful of high doses.

FDA announces new safety recommendations for high-dose simvastatin - 80

http://www.newswise.com/articles/can-high-dose-statins-improve-outcomes-after-aneurysm-related-stroke
Can treatment with high doses of a cholesterol-lowering statin drug improve outcomes for patients with stroke caused by rupture and bleeding of brain aneurysms? An ongoing clinical trial will soon find out, according to an article in the May issue of Neurosurgery, official journal of the Congress of Neurological Surgeons. The journal is published by Lippincott Williams & Wilkins, a part of Wolters Kluwer Health.
Together with other research already underway, the trial will help to determine whether statin medications are effective in limiting damage to the brain in patients with aneurysmal subarachnoid hemorrhage (SAH). The lead investigator is Dr. George Kwok Chu Wong of Chinese University of Hong Kong.
Statins Show Promise in Treatment of Aneurysmal SAH
Dr. Wong and colleagues outline their plans for a study to evaluate the benefits of high-dose simvastatin for patients with SAH caused by a ruptured aneurysm. Subarachnoid hemorrhage is a life-threatening type of stroke in which there is bleeding into the brain. It most commonly occurs when an aneurysm—a weak spot in one of the blood vessels supplying the brain—ruptures or breaks.
Experimental studies, including preliminary studies in humans, have suggested that simvastatin may have treatment benefits for SAH. Statins have known "neuroprotective" effects in brain tissue. A recent summary of the evidence suggests that simvastatin—a widely prescribed cholesterol-lowering drug—can reduce brain injury caused by delayed ischemia (decreased blood flow). Delayed ischemia is a major contributor to death and disability after SAH.
Based on the evidence, statins have been recommended as part of routine treatment for aneurysmal SAH. "However," Dr. Wong and coauthors write, "no clinical data are available to answer whether a high-dose regimen is more effective than a normal-dose regimen, even though the biochemical actions and related neuroprotective mechanisms are thought to be dose-related."
Trial to Compare High vs Low Doses of Simvastatin
The planned study will compare high-dose versus low-dose simvastatin for patients with aneurysmal SAH. Both the higher and lower doses—80 and 40 milligrams per day—are commonly used in treating high cholesterol. Patients will be randomly assigned to either the higher or lower dose; treatment will start within 96 hours after stroke onset and continue for three weeks.
The main objective will be to see if there's any difference in the rate of delayed ischemia causing brain damage between groups. The study will also look for between-group differences in neurological function and disability, and evaluate the cost-effectiveness of high- versus low-dose simvastatin treatment. Safety assessment will include special attention to the risk of certain statin-related complications in the higher-dose group.
Dr. Wong and colleagues have been enrolling patients in their trial, and expect to have the results soon. They note that another trial is being conducted to compare normal-dose simvastatin with inactive placebo for patients with SAH after ruptured aneurysm. They conclude, " When the results are interpreted together, the research question of a possible beneficial effect of high-dose simvastatin in acute aneurysmal subarachnoid hemorrhage could be answered."

Could eating less save your brain? Study shows reducing calories delays nerve cell loss

Ask your doctor and researchers if immediately after your stroke you should reduce calorie consumption to try to save your damaged neurons.  Why don't they know anything about this idea?
http://www.foxnews.com/health/2013/05/22/could-eating-less-save-your-brain-study-shows-reducing-calorie-intake-delays/?intcmp=obnetwork
Calorie restriction may not always be fun, but cutting back has benefits beyond even weight loss. Studies have shown that eating less can help slow aging, prolong life and even decrease the effects of diseases like Alzheimer’s in a variety of organisms.

Based on this knowledge, a group of researchers from the Massachusetts Institute of Technology (MIT) decided to dig further and ask: Could calorie restriction also delay nerve cell loss in the brain – and the changes in learning and memory that go along with it?

“We reasoned – and other folks reasoned – that because cognitive decline and neurodegeneration are characteristics of the aging process, that calorie restriction might also work in the brain to slow neurodegeneration,” lead study author, Dr. Johannes Gräff from the Picower Institute for Learning and Memory at MIT, and Howard Hughes Medical Institute, told FoxNews.com.

Read more: http://www.foxnews.com/health/2013/05/22/could-eating-less-save-your-brain-study-shows-reducing-calorie-intake-delays/?intcmp=obnetwork#ixzz2U36JqZWB

 

More at link.

The Soaring Cost of Stroke

And the incorrect response is to suggest more stroke education like this;
While an aging population is at the core of the problem, stroke education may help avert a crisis.

"Exercise regularly and eat healthy to help prevent stroke." Press releases, bah.

http://www.dailyrx.com/stroke-costs-are-projected-double-number-people-having-strokes-increases 

What should be done is figure out how to stop the neuronal cascade of death. That would prevent lots of disability and increase the 10% full recovery to something reasonable. 

 

Can Statins Cut the Benefits of Exercise?

A great question for your doctor.
The New York Times writeup here:
http://well.blogs.nytimes.com/2013/05/22/can-statins-curb-the-benefits-of-exercise/
The abstract here:
Simvastatin impairs exercise training adaptations

7 years and counting

I'm still around and kicking, the first day was touch and go. I've come to the conclusion that rehabbing stroke associations should be easy, with something like that that is so badly run it should be easy to correct as compared to a smoothly running organization. Although it is smoothly running but not doing anything.

Folic acid decreases stroke risk

And this one can get you to a 337% reduction in stroke risk.
http://www.alberniportal.ca/2013/05/folic-acid-decreases-stroke-risk/
A study shows that men who consume large amounts of folic acid have a reduced risk of stroke.
Previous research have pointed to the health benefits of an adequate intake of the B vitamin folic acid (sometimes also called folate). It seems to work by preventing the build up of the amino acid homocysteine which otherwise damages the arteries.
Researchers at Northwestern University in Illinois followed a group of nearly 44,000 men for 14 years, noting their folic acid intake. Folic acid can be taken by supplement and it is also found in grains (now fortified following US Government advice), fruits and vegetables. In this study, men taking the most folic acid – half of whom had an intake of over 821 micrograms a day – had a 30 per cent lower risk of ischemic stroke compared to those consuming around 262 micrograms of folic acid a day, or less. An ischemic stroke is one which is caused by a blood clot in the brain, while a hemorrhagic stroke is caused by bleeding. There was no link between folic acid intake and hemorrhagic stroke.

Previous ones here;
http://oc1dean.blogspot.com/2013/03/stroke-risk-reduction-ideas.html