Brain exercises may curb cognitive impairment

'May' is not good enough. What the hell will it take to get to an exact level of specificity?

Brain exercises may curb cognitive impairment

Reuters Health News | March 27, 2020

Exercises aimed at improving vision-based speed of processing (VSOP) and other brain functions may slow the progress of mild cognitive impairment, according to New York-based researchers.

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"VSOP training strengthens cognitive and neural efficiency, with concomitant vagal regulation of cardiac control, suggesting overall better capacity for adaptation to stress," Dr. Feng V. Lin and colleagues at the University of Rochester, in New York, write in Neuroimage.
As Dr. Lin told Reuters Health by email, "the brain-heart relationship is important; cardiovascular function-driven stress regulation, an important capacity for living and thriving, can be enhanced by brain training in old age."
She and her colleagues studied 84 older adults (mean age, 74.7), all of whom had amnestic mild cognitive impairment (aMCI). Following baseline assessment, participants were randomly assigned 2:1 to VSOP or to active-control mental leisure activities (MLA). Participants in each group were encouraged to train for 6 weeks, completing four 1-hour sessions each week.
Outcome assessors and participants were blinded to group randomization. The MLA group played online games including word search, Sodoku and Solitaire. The other participants engaged in a suite of five BrainHQ (Posit Science) exercises aimed at boosting processing speed and attention (PS/A).
For example, in one of these exercises, called Hawks Eye, a cluster of birds briefly flashed on to the screen in peripheral vision and participants had to identify the one target bird that differed from the others.
Using a variety of measures including resting and cognitive task-based ECG, and resting fMRI pre- and post-intervention, "we aimed to test whether PS/A causally influences vagal control of the autonomic nervous systems via their shared central neural pathways in aMCI," the researchers write.
Compared with controls, they found that changes in PS/A and salience-network connectivity "significantly predicted change in high frequency heart rate variability from baseline to post-test and/or 6-month-follow-up." Age, neurodegeneration, or gender did not affect these relationships.
Interventions in PS/A, they conclude, "may be a viable approach for promoting adaptation capacity in groups at risk for dementia."
Dr. Henry Mahncke, CEO of Posit Science, told Reuters Health by email that "this is an encouraging science-based message of hope for people with this condition (aMCI), who might feel that their brains are on an inevitable path of decline."
But, added Dr. Mahncke, who was not involved in the research, "that's not the case—these results show that people with aMCI have brains that are still capable of positive change with the right kind of brain training. And of course, the same is true for normal cognitive aging, where many large scale trials show that people can improve their brain function and cognitive function with brain training."
The study had no commercial funding, and the researchers report no conflicts of interest.
—David Douglas

To read more, click here.

Electrical 'storms' and 'flash floods' drown the brain after a stroke

To me, this means the goal for tPA administration is 3 minutes after stroke onset. 'Think your stroke team can do that?' Since you will never meet that goal you are going to have to go down the difficult route of solving the 5 causes of the neuronal cascade of death in the first week. 100% recovery is still expected.

Electrical 'storms' and 'flash floods' drown the brain after a stroke

Salty fluid regularly flushes through the brain to clear away toxins and waste, but after a stroke, this liquid floods the organ, drowning its cells.
Swelling in the brain, known as cerebral edema, occurs after stroke as water flows into brain cells and the space surrounding them. For years, scientists thought this excess fluid came from blood, but new evidence suggests that the water springs from another source entirely: the sodium-rich cerebrospinal fluid that permeates the brain. These results come from both live mouse models and human tissue.

The findings, published Jan. 30 in the journal Science, point to potential treatments to subdue swelling in the brain and improve patients' recovery after stroke.
Related: From Dino Brains to Thought Control — 10 Fascinating Brain Findings

CLOSE

Wash cycle gone wrong

Strokes occur when a blockage plugs a blood vessel in the brain, or a vessel completely ruptures. Without an adequate energy supply, brain cells can no longer police which particles pass through their membranes. Within minutes, the neurons swell like overfilled beach balls and begin to short-circuit, accrue damage and die. Hours later, the tightly woven tissue lining blood vessels in the brain, the blood-brain barrier, also begins to malfunction, and the entire organ takes on water.
"For over 60 years, people thought this accumulation of fluid was coming from the blood" leaking through the compromised blood-brain barrier, said study lead author Dr. Humberto Mestre, a clinician and current doctoral student at the University of Rochester Medical Center (URMC) Center for Translational Neuromedicine. But cerebral edema sets in long before the blood-brain barrier breaks down, leading Mestre and his colleagues to wonder whether the water actually comes from somewhere else.
"No one had looked at these alternate fluid sources," Mestre said. Cerebrospinal fluid, which makes up about 10% of the fluid found in the mammalian cranial cavity, stood out as a promising candidate, he added.
In the brain, cerebrospinal fluid flows through the glymphatic system, a network of tubing that winds along paths carved out by the organ's veins and arteries, according to a 2015 report in the journal Neurochemical Research. The fluid flows just outside the blood vessels, held in place by a "doughnut-shaped tunnel" of cells. (Picture a length of wire, representing an artery, resting inside a rubber hose, which acts like the outer tunnel filled with fluid.) As muscles along the arteries contract, the nearby cerebrospinal fluid gets pushed along its route and picks up metabolic wastes on the way. Besides taking out the trash, the glymphatic system may also help distribute fats, sugars and other important compounds within the brain.
Although crucial in a healthy brain, in the aftermath of a stroke, the glymphatic system goes haywire and drives the onset of edema, Mestre and his co-authors found. "The cerebrospinal fluid is actually the primary driver of swelling right after the stroke happens," Mestre said.

Staying the flood

The role of cerebrospinal fluid in stroke eluded scientists for decades, in part, because no technology existed to observe a stroke unfolding in real time, Mestre said.
He and his co-authors combined several techniques to observe the change in fluid flow in mice experiencing stroke. The team peered into the animals' brains using both MRI and a two-photon microscope, which uses light and fluorescent chemicals to image living tissues. "We can basically image what the cerebrospinal fluid is doing while the stroke is happening," Mestre said. By infusing the fluid with radioactive particles, the researchers could also determine how the flow rate changed over time.
Using these methods, the team determined that edema takes hold of the mouse brain "as early as 3 minutes" after stroke, long before the blood-brain barrier began to leak, Mestre said. As brain cells short-circuit, they spew chemical messengers known as neurotransmitters and potassium into the space beyond their membranes. Nearby cells react to the influx of chemicals and, in turn, short-circuit. As these electrical storms sweep through the brain, muscles within the blood vessels contract and create a pocket of space between themselves and the surrounding glymphatic system. Salty cerebrospinal fluid gets sucked into the resulting vacuum, pulling water molecules along with it.
"Wherever sodium is accumulating, water is going to follow it," Mestre said. The team could watch this game of follow-the-leader unfold in select areas of the brain but could not track water flow in the whole organ at once. Using a computer model to simulate the entire glymphatic network, however, they were able to predict how constricting blood vessels would drive the flow of water through a whole mouse brain after stroke.
To connect the dots between mice and humans, the authors examined the brain tissue of patients who had died from ischemic stroke, wherein a blood clot blocks a blood vessel in the brain. The mouse and human brains accumulated fluid in the same regions, namely areas through which the glymphatic system runs and picks up wastes. Given the strong correlation between animals and people, "these findings could provide a conceptual basis for development of alternative treatment strategies," the authors noted.
The team tested one of these strategies in mice by blocking a water channel on astrocytes, cells in the brain that help direct water through the glymphatic system. Mice that lacked the channel were slower to develop edema after stroke, suggesting that a similar treatment could show promise in human patients. In addition to blocking water flow, future treatments could potentially prevent edema by slowing the spread of stroke-induced electrical activity in the brain, the authors added. These electrical storms continue to barrage the brain for days after stroke, inciting edema each time they happen.
The harmful waves of electrical activity seen in ischemic stroke also appear in concert with "virtually every [central nervous system] injury," Mestre said. The new study hints that the glymphatic system may play roles in conditions where there's bleeding in and around the brain, traumatic brain injury and even migraine, although such connections remain "purely speculative." Someday, the glymphatic system could offer doctors a whole new strategy for treating acute brain injuries, Mestre said.

Originally published on Live Science.

Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation

In the three years since this came has a protocol been created on this method?

ASK YOUR DOCTOR AND NOT POLITELY, if not there, start screaming in their faces; 'WHY IS THERE SO MUCH FUCKING INCOMPETENCY IN STROKE?' We have to let the stroke medical world know they are on notice to deliver 100% recovery and we are watching them. They don't even know that 100% recovery is the stated goal of all survivors. You will get the tyranny of low expectations from them; 'You'll be lucky if you walk again.' DEMAND RUNNING PROTOCOLS IF YOU GET THAT SHIT!

Targeting interhemispheric inhibition with neuromodulation to enhance stroke rehabilitation

 L.J. Boddington, J.N.J. Reynolds

 Article history:
Received 26 February 2016Received in revised form10 December 2016Accepted 10 January 2017Available online xxx
Keywords:
Interhemispheric inhibition Stroke Rehabilitation Neuromodulation Transcranial magnetic stimulation Electrical stimulation

a b s t r a c t

Background/Objectives:
 Interhemispheric inhibition in the brain plays a dynamic role in the production of voluntary unimanual actions. In stroke, the interhemispheric imbalance model predicts the presence of asymmetry in interhemispheric inhibition, with excessive inhibition from the contralesional hemisphere limiting maximal recovery. Stimulation methods to reduce this asymmetry in the brain may be promising as a stroke therapy, however determining how to best measure and modulate interhemispheric inhibition and who is likely to benefit, remain important questions.
Methods:
 This review addresses current understanding of interhemispheric inhibition in the healthy and stroke lesioned brain. We present a review of studies that have measured interhemispheric inhibition using different paradigms in the clinic, as well as results from recent animal studies investigating stimulation methods to target abnormal inhibition after stroke.
Main findings/Discussion:
 The degree to which asymmetric interhemispheric inhibition impacts on stroke recovery is controversial, and we consider sources of variation between studies which may contribute to this debate. We suggest that interhemispheric inhibition is not static following stroke in terms of the movement phase in which it is aberrantly engaged. Instead it may be dynamically increased onto per-ilesional areas during early movement, thus impairing motor initiation. Hence, its effect on stroke recovery may differ between studies depending on the technique and movement phase of eliciting the measurement. Finally, we propose how modulating excitability in the brain through more specific targeting of neural elements underlying interhemispheric inhibition via stimulation type, location and intensity may raise the ceiling of recovery following stroke and enhance functional return.
©
 2017 Elsevier Inc. All rights reserve

The impact of white wine on your health

Your doctor will never tell you about this benefit, you'll get this instead. Of course you'll have to figure out the dose needed yourself. 

Safest level of alcohol consumption is none, worldwide study shows

Or maybe you prefer red wine:

Benefits of red wine—health or hype?

 

The latest here:

 

The impact of white wine on your health

Melissa Sammy, MDLinx | March 26, 2020

Red wine, a distinguished component of (arguably) the healthiest diet in the world—the Mediterranean diet—is often extolled for its numerous health benefits. These benefits are owed to red wine’s naturally occurring key ingredients: heart-healthy antioxidants, cholesterol-lowering polyphenol resveratrol, and anti-cancer polyphenol ellagic acid. But—what about white wine?

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Researchers have shown that white wine has its own unique roster of health-boosting chemicals and antioxidants that sets it apart from red wine.

Although not as extensively studied as its red counterpart, white wine does have some positive health attributes. In fact, some researchers have shown that white wine has its own unique roster of health-boosting chemicals and antioxidants that sets it apart from red wine.
So, whether you’re allergic to red wine, not a big fan of the taste, are searching for something light and refreshing for the warm-weather months, or just outright prefer white wine, here are five health benefits of white wine that may inspire you to pour a glass:
Heart health and metabolism. Researchers have shown that drinking white wine may improve cardiovascular and metabolic function. In one study, researchers randomized 224 patients with well-controlled type 2 diabetes to drink either red wine, white wine, or mineral water with their dinners for 2 years to determine the effect of moderate wine intake. At the end of the trial, although red wine drinkers demonstrated the most improvements in lipid and glucose control, those who drank white also saw improvements. Plus, compared with those who drank mineral water, white wine drinkers saw no increases in blood pressure levels or decreases in liver function.
In another study, drinking aged white wine(You could ask your doctor the definition of aged, whites are usually not aged like reds.) brought about greater heart-health benefits than drinking gin. In fact, white wine helped to repair endothelial cells lining blood vessels, thus offering cardioprotection. It also decreased the presence of inflammatory cells and pro-inflammatory biomarkers.

• See Also: The healing powers of beer

Lung health. This is one area of health where white wine may have an edge over red. While white and red wine can both bolster lung function, white wine seems to have a greater positive impact on it.
In one study by University of Buffalo researchers, 1,555 participants were assessed for lifetime alcohol consumption, lifestyle habits, body measurements, and lung function. According to findings, wine drinkers had the highest concentration of protective antioxidants in their blood. Additionally, following an analysis of all alcohol intake variables with lung function, both recent and lifetime intake of wine had the strongest associations with volume forcibly expelled in one second and forced vital capacity. Interestingly, this association was stronger for white wine.
“Red wine in moderation has been shown to be beneficial for the heart, but in this case the relationship was stronger for white wine. We also have shown that both dietary levels and blood serum levels of antioxidants are linked to lung health and function. We think that the antioxidants in wine account for our current findings,” said study author Holger Schünemann, MD, PhD.
Renal health. One unique compound in particular—caffeic acid—may be responsible for white wine’s health benefits, according to researchers. For instance, in a study published in PLOS ONE, Italian researchers isolated and investigated caffeic acid for its purported antioxidant activities. Specifically, they assessed the protective effect of low-dose caffeic acid on oxidative stress-induced endothelial injury. Overall, low-dose caffeic acid—similar to the amount observed following moderate white wine consumption—may offer endothelial protection and reduce the risk of cardiovascular and kidney disease.

• See Also: Wine before beer? Researchers test age-old adage

Cognitive health. Some researchers have shown that the unique antioxidants specific to white wine may offer protection against cognitive decline. For instance, in a study published in the Journal of Nutritional Biochemistry, researchers extracted polyphenols from white wine and fed them to mice for 2 months to determine the impact of a white wine-enriched diet on the brain for Alzheimer disease-like pathology. At the end of the trial, these mice had lower risk of developing cognitive problems leading to Alzheimer disease.
Glycemic health. Like red wine, white wine may help improve cholesterol levels. In one study involving 146 participants with mild to moderate risk of cardiovascular disease who were followed for a year, those who exercised at least two times per week and drank wine―white or red―saw significant improvements in their LDL cholesterol levels.
As always, remember that moderation is key and to drink responsibly. Cheers!

Survivors of chronic stroke experience continued impairment of dexterity but not strength in the nonparetic upper limb

I got nothing useful out of this, generic blathering. 

Survivors of chronic stroke experience continued impairment of dexterity but not strength in the nonparetic upper limb

Archives of Physical Medicine and Rehabilitation — Barry AJ, et al. | March 25, 2020

Researchers assessed the performance of the less affected upper limb among individuals with stroke relative to normative values. They evaluated less affected upper limb function among those whose prestroke dominant limb became paretic and those whose prestroke nondominant limb became paretic in this cohort analysis of survivors of chronic stroke (7.2 ± 6.7y post incident). Even years post-stroke, significant upper extremity impairment in the nominally nonparetic limb was identified among survivors of stroke with severe impairment of the paretic limb, irrespective of whether the dominant hand or nondominant hand was primarily affected. Since this group of survivors of stroke particularly rely on the nonparetic limb for performing functional tasks, targeting the nonparetic upper limb for rehabilitation was recommended.(Useless, we need specifics, not this generic crapola.)

Read the full article on Archives of Physical Medicine and Rehabilitation

Squishy Low-Cost Sensors to Monitor Stroke or Sporting Injury Victims

This is the only way your therapists will be able to objectively determine your movement impairments. From that you could start creating protocols that fix such impairments. But nothing like that will occur because we don't have two functioning neurons in all of stroke leadership.  You're screwed.

Squishy Low-Cost Sensors to Monitor Stroke or Sporting Injury Victims

25-03-2020 |   |  By Rob Coppinger

Reliable, portable, rubber bonded low-cost electrical components could be fitted to stroke or sports injury victims’ bodies as part of their rehabilitation at home.

Imperial College London (ICL) researchers have invented a way to bond a stretchy and squeezy force-sensitive soft material to electrical components. They created a bond between the soft material and components that is so strong the stretchy rubber material breaks before the bond between the components and rubber does. Adhesives have been used previously to try to bond the rubber material, which is conductive, to electrical components, but they broke down when the two materials were pulled apart. 

“We hope [our] method will allow us to make low-cost soft sensors that are reliable and portable, that can be used to monitor people’s health in their own homes,” said ICL Department of Bioengineering researcher, Michael Kasimatis. “Such sensors could be coupled with a mobile device, such as a smartphone so that the data they generate can be easily processed and stored on the cloud, which is important for applications in digital healthcare.”

Stretchy Resistance 

The ICL researcher’s new method is to use metal-coated silicon which triggers a chemical bond with the stretchy and squeezy rubber. The silicon contacts are smooth on one side, where they bond to the rubber, and pitted and plated with copper on the other side, so wires or other electric components can be easily attached using conventical methods, such as soldering. The ICL research team is seeking partners to advance technology.

The Squishy Sensor

A few healthcare and rehabilitation prototype sensors have been tested to demonstrate how the bonding method can resist the strains of repeated stretching. The prototypes included a wearable breathing monitor, a leg band for exercise monitoring and a squeezy ball for hand rehabilitation. A squeezy ball is viewed as a potentially very useful rehabilitation tool and soft electrical force sensor as it can be used by patients with hand injuries or neurological disorders.

While such sensors have been in development for a long time, none have been commercialised because it has been difficult to integrate them with the electronic components, such as the wires, microchips and the batteries; all of which are needed to collect, process, analyse and transmit the data the sensor has been collecting. With the successful demonstration of the new bonding technique and its application to laboratory prototypes, the research team are planning to take the technology out of the lab and commercialise it.

 

---

By Rob Coppinger

Rob Coppinger is a freelance science and engineering journalist. Originally a car industry production engineer, he jumped into journalism and has written about all sorts of technologies from fusion power to quantum computing and military drones. He lives in France.

New Chapter in NWI Stroke Recovery Begins with $40M Stroke and Rehabilitation Center Project Completion - Crown Point, IN

But are you going to provide the same results of FAILURE, FAILURE, FAILURE? Your choice, ask them the hard questions or accept fucking failures. All I see is 'care' which means absolutely nothing.

Three measurements will tell me if the stroke hospital is possibly not completely incompetent; DO YOU MEASURE ANYTHING?

1. tPA full recovery? Better than 12%?
2. 30 day deaths? Better than competitors?
3. rehab full recovery? Better than 10%?

 

New Chapter in NWI Stroke Recovery Begins with $40M Stroke and Rehabilitation Center Project Completion

Posted By

leslie

-

March 25, 2020

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Community Stroke and Rehabilitation Center located at 10215 Broadway in Crown Point, IN

Patients regaining their strength after strokes and other medical conditions have a brand-new state-of-the-art facility for their recovery.
The Pangere Corporation, a commercial and industrial contractor based in Gary, IN, recently announced the construction of Community Healthcare System’s new specialty hospital in Crown Point. The $40 million Community Stroke & Rehabilitation Center recently has been completed and is now serving the community.
“This beautiful new building is a great place for recovery, rehabilitation and already has a reputation for tough therapists,” joked one recent stroke survivor. His goal is to walk unassisted by this summer, a little over a year after his stroke. Medical staff at the new building are working to see that he does.
“That’s why we do what we do,” said Steve Pangere, President of the Pangere Corp. “We’re proud to deliver project outcomes that serve people well. The new Community Stroke & Rehabilitation Center is going to improve the quality of life for a lot of people for years to come.”
Crown Point Mayor David Uran said, “The builders of this facility had the future in mind. We’re thrilled with the outcome, and the expansion of world-class care in our city.”
Four Floors of Healing
The facility is a four-story, 129,000-square-foot multispecialty center that features inpatient rehabilitation, therapy gyms, and living-skills space. In addition, outpatient services include immediate care, a full lab, diagnostic testing and imaging services, and a Women’s Diagnostic Center.
Community Care Network specialists in cardiology, internal medicine, neurology, obstetrics and gynecology, orthopedics, and pulmonary medicine broaden the scope of wellness and preventative care.
The first floor of the new Stroke & Rehabilitation Center contains immediate care, radiology, CT, MRI, non-invasive cardiology testing, laboratory services, and outpatient therapy services including physical therapy, occupational therapy, speech therapy, and physician offices.
The second floor houses the Women’s Diagnostic Center which offers bone density scanning, mammography, ultrasound, and other services.
The third and fourth floors have 40 private rooms for inpatient rehabilitation care. Among those are apartment-themed rooms where patients can practice daily living activities. Therapies provided on these floors are for complex stroke, traumatic brain injury, neurological conditions, and spinal cord treatments.
The building also has a healing garden, a visitors’ café and an abundance of natural lighting.
High-Quality Craftsmanship 
Hundreds of union craft workers helped bring the facility to life. The Pangere Corp. worked with a team of about 38 subcontractors and numerous suppliers. Only the most modern building materials, equipment and finishes were incorporated into the building’s design. The architect for the project was Design Alliance Architects from Hammond, IN.
All Pangere Corp. carpenters are certified in Infection Control Risk Assessment (ICRA) and are accredited fire stop installers. Additionally, the company recently became one of just a few midwestern contractors to earn Door Safety Inspector (DSI) certifications from the National Fire Protection Association (NFPA).
For details and information about services offered at the Community Stroke & Rehabilitation Center, visit: https://www.comhs.org/about-us/community-stroke-and-rehabilitation-center.

Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6

Now we just need someone competent that can create a protocol to deliver suppression of TRPC6 channel degradation. But with NO STROKE LEADERSHIP, nothing will occur. You, your children and grandchildren are fucking screwed.  

Novel Targets for Stroke Therapy: Special Focus on TRPC Channels and TRPC6

Lu Liu¹, Lijuan Gu², Manli Chen¹, Yueying Zheng¹, Xiaoxing Xiong^1,2* and Shengmei Zhu^1*

• ¹Department of Anesthesiology, The First Affiliated Hospital, College of Medicine, Zhejiang University, Hangzhou, China
• ²Central Laboratory, Renmin Hospital of Wuhan University, Wuhan, China

Stroke remains a leading cause of death, disability, and medical care burden worldwide. However, transformation from laboratory findings toward effective pharmacological interventions for clinical stroke has been unsatisfactory. Novel evidence has been gained on the underlying mechanisms and therapeutic potential related to the transient receptor potential (TRP) channels in several disorders. The TRP superfamily consists of a diverse group of Ca²⁺ permeable non-selective cation channels. In particular, the members of TRP subfamilies, TRP canonical (TRPC) channels and TRPC6, have been found in different cell types in the whole body and have high levels of expression in the central nervous system (CNS). Notably, the TRPCs and TRPC6 channel have been implicated in neurite outgrowth and neuronal survival during normal development and in a range of CNS pathological conditions. Recent studies have shown that suppression of TRPC6 channel degradation prevents ischemic neuronal cell death in experimental stroke. Accumulating evidence supports the important functions of TRPC6 in brain ischemia. We have highlighted some crucial advancement that points toward an important involvement of TRPCs and TRPC6 in ischemic stroke. This review will make an overview of the TRP and TRPC channels due to their roles as targets for clinical trials and CNS disorders. Besides, the primary goal is to discuss and update the critical role of TRPC6 channels in stroke and provide a promising target for stroke prevention and therapy.

Introduction

Ischemic stroke is induced by the obstruction of an artery or multiple arteries leading to the brain. Focal impairment or occlusion of blood circulation to the brain impairs the normal function of neurons. The mechanisms underlying ischemic stroke are complex, and include excitotoxicity, oxidative and nitrosative stress, Ca²⁺ overload, inflammation, and apoptosis (Szydlowska and Tymianski, 2010; Khoshnam et al., 2017). Among these mechanisms, intracellular Ca²⁺ overload remains a vital role in neuronal injury associated with ischemic stroke (Choi, 1995). Glutamate receptors, such as N-methyl-D-aspartate receptor (NMDAR), are thought to be major pathways for intracellular Ca²⁺ influx in the central nervous system (CNS) after cerebral ischemia-reperfusion (IR) injury. Excessive NMDARs activation and the following Ca²⁺ influx through NMDARs are crucial steps required for initiating ischemic cell death (Szydlowska and Tymianski, 2010; Lai et al., 2011). To date, pre-clinical studies have provided substantial evidences for the neuroprotective effect of NMDAR antagonists in experimental ischemic stroke (Ginsberg, 2008). However, for several decades, clinical trials of NMDAR antagonists have all ended up with failure to show beneficial effects due to their narrow therapeutic windows and adverse effects (Wu and Tymianski, 2018). Thus, effective therapeutic interventions for ischemic stroke are urgently required.

Despite the pivotal functions of NMDARs, non-glutamate mechanisms have drawn attention as promising Ca²⁺ influx pathways involved in brain ischemia. In this respect, researchers shifted focus toward the transient receptor potential (TRP) channels (Szydlowska and Tymianski, 2010). TRPs are non-selective cationic channels which have key functions in different disorders (Moran, 2018). The TRP canonical (TRPC) subfamily was proved to be extensively distributed in CNS and have important functions in neuronal development (Tai et al., 2009). Understanding of these channels may drive the researchers to make a significant breakthrough in CNS diseases therapy. Recently, growing evidence indicates that TRPC6 channel has been involved in Ca²⁺ homeostasis and shown to participate in the molecular pathophysiology of ischemic stroke. TRPC6 was reported to have an critical role in neuroprotection in both in vitro and in vivo models of ischemic stroke (Du et al., 2010). In this review, we present a general description of the current understanding of TRPs and TRPC subfamily, with an emphasis on their involvement in clinical trials and CNS dysfunctions. Furthermore, this review concentrates on evidence-based advancements of TRPC6 in CNS disorders and cerebral ischemia. The primary aim is to clarify the relationship between TRPC6 and ischemic stroke and discuss future perspectives.

More at link. 

Do you know how to interpret clinical trial results?

Of course not, that is your doctor's job. Are they good at it? I've listed thousands that your doctor and stroke hospital should have interpreted and created stroke protocols. HAVE THEY DONE A SINGLE ONE?

Do you know how to interpret clinical trial results?

STAT’s guide to interpreting clinical trial results

$499.00

License Type: Individual Group

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Interpreting clinical trial results is not for the faint of heart. Companies spin, short-sellers hawk, and everyone else is left swimming through the muck. But there is an art to reading, and writing, scientific results — and you can learn it.

In our latest STAT Report, STAT senior writers Sharon Begley and Adam Feuerstein provide basic tools to help you read clinical trial results with an appropriately skeptical (or at least critical) eye. They also examine specific examples of spin, noting the sections of papers reporting the results of clinical trials where they appear — and why that matters. If you’re looking to cut through noise to better understand scientific data or make sense of company performance and value, this report will give you the foundation you need to make smarter business decisions.
Highlights include:

• A definition of spin in clinical trials, supported by real life examples.
• Four key questions to ask when evaluating clinical trial results, and an overview of additional tools you need to read results more critically
• Analysis of the red flags you should look for in clinical trial design, execution, and reporting of results.

How it works

Add this report to your cart, and then complete the checkout process. Once you have, you'll receive an email with the link to download the full report file. This report is digital-only, so you will not receive a printout.

Preview

Take a peek at what's included in this report.

The role of amantadine in cognitive recovery early after traumatic brain injury: a systematic review

WHOM is going to do the followup to see if this would help in stroke also? Nothing will occur since we have NO STROKE LEADERSHIP to contact with these suggestions.

The role of amantadine in cognitive recovery early after traumatic brain injury: a systematic review

Author links open overlay panelAndreaLoggini

RuthTangonanFatenEl AmmarAliMansourFernando DGoldenbergChristopher L.KramerChristosLazaridis

https://doi.org/10.1016/j.clineuro.2020.105815Get rights and content

Highlights

•

Cognitive dysfunction is a common sequela of traumatic brain injury.

•

Amantadine has been investigated in cognitive recovery after traumatic brain injury.

•

Amantadine is well tolerated; may hasten cognitive recovery in the intermediate-term.

•

Efficacy of amantadine in improving long-term cognitive recovery remains uncertain.

Abstract

We conducted an updated systematic review on the safety and efficacy of amantadine in cognitive recovery after traumatic brain injury (TBI), in order to determine if the current literature justifies its use in this clinical condition. A comprehensive search strategy was applied to three databases (PubMed, Scopus, and Cochrane). Only randomized clinical trials (RCTs) that compared the effect of amantadine and placebo in adults within 3 months of TBI were included in the review. Study characteristics, outcomes, and methodological quality were synthesized. This systematic review was conducted and presented in accordance with the Preferred Reporting Items for Systematic Reviews and Meta-Analyses (PRISMA). A quantitative synthesis (meta-analysis) was not feasible due to the large heterogeneity of studies identified.

Three parallel RCTs and one cross-over RCT, with a total of 325 patients were included. All of the studies evaluated only severe TBI in adults. Amantadine was found to be well tolerated across the studies. Two RCTs reported improvement in the intermediate-term cognitive recovery (four to six weeks after end of treatment), using DRS (in both studies) and MMSE, GOS, and FIM-Cog (in one study). The effect of amantadine on the short-term (seven days to discharge) and long-term (six months from the injury) cognitive outcome was found not superior to placebo in two RCTs. The rate of severe adverse events was found to be consistently very low across the studies (the incidence of seizures, elevation in liver enzymes and cardiac death was 0.7%, 1.9%, and 0.3%, respectively). In conclusion, amantadine seems to be well tolerated and might hasten the rate of cognitive recovery in the intermediate-term outcome. However, the long-term effect of amantadine in cognitive recovery is not well defined and further large randomized clinical trials in refined subgroups of patients are needed to better define its application.

Recombinant Human Growth Hormone Ameliorates Cognitive Impairment in Stroke Patients

What is your doctor doing to recover your 5 lost cognitive years from your stroke? 

Did your doctor and stroke hospital do one damn thing with all this earlier research? I'd suggest mass firings.

Growth Hormone Improves Cognitive Function After Experimental Stroke

April 2018

Growth Hormone (GH) Administration Increases the Metabolic Activity of the left Hippocampus in an Elder Patient with Cognitive Disorders

May 2018

Growth hormone could play critical role in stroke rehabilitation and recovery, Hunter researchers say

 

May 2018

Brain fertiliser nurtures new hope for stroke survivors

September 2018

11 Ways to Boost Human Growth Hormone (HGH) Naturally

September 2018 

This is your doctor's responsibility, don't let her/him wash their hands of it and ignore the problem they caused by doing nothing to stop the 5 causes of the neuronal cascade of death in the first week. 

The latest here:

Recombinant Human Growth Hormone Ameliorates Cognitive Impairment in Stroke Patients

Xuewen Feng;Guanwu Li;Weilin Wu;Yongming Xu;Haiyang Lin;Jingzheng Fan;

+ Author Information

Check Ovid for access

View on Journal Site

Abstract

Objective 

We aimed to determine the effects of recombinant human growth hormone (rhGH) replacement on cognitive function in subjects with poststroke cognitive impairment using resting-state functional magnetic resonance imaging. 

Methods 

We included 60 patients with a first-ever stroke for 3 months and a diagnosis of cognitive impairment who were randomized 1:1 to receive either rhGH subcutaneously or placebo injection for 6 months. All subjects were required to receive the same rehabilitative therapy program. Both groups were subjected to pretreatment and posttreatment neuropsychological assessment using the Montreal Cognitive Assessment, serum neurotrophic factors, biomarkers of glucose and lipid metabolism, and functional magnetic resonance imaging during 6 months of the study period. The pattern of brain activity was determined by examining the functional connectivity and amplitude of low-frequency fluctuations (ALFF) of blood oxygen level dependent signal. 

Results 

Forty-three (82.7%) completed the study. Treatment with rhGH reduced levels of triglycerides and low-density lipoprotein cholesterol but did not significantly altered plasma concentrations of glucose and glycated hemoglobin. We found a significant increase in serum insulin-like growth factor 1 levels (32.6%; P < 0.001) in the rhGH-treated group compared with that in the controls. After 6 months of rhGH treatment, mean Montreal Cognitive Assessment score improved from 16.31 (5.32) to 21.19 (6.54) (P < 0.001). The rhGH group showed significant increased area of activation with increased ALFF values in the regions of the frontal lobe, putamen, temporal lobe, and thalamus (P < 0.05), relative to the baseline conditions. The correlation analysis revealed that the ALFF and functional connectivity of default mode network was positively correlated with the ΔMoCA score and ΔIGF-1 levels; that is, the more the scale score increased, the higher the functional connection strength. No undesirable adverse effects were observed. 

Conclusions

The rhGH replacement has a significant impact on global and domain cognitive functions in poststroke cognitive impairment.

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Analysing Patients Shortly After Stroke Can Help Link Brain Regions to Speech Functions

Well good, calling for more research based on this analysis. It will never occur, WE HAVE NO STROKE LEADERSHIP AND NO STROKE STRATEGY.  All this stroke research is a waste of time and money since no one is connecting the dots to get stroke survivors to 100% recovery. Stroke is a complete fucking failure and I don't see that changing unless survivors are in charge. 

Analysing Patients Shortly After Stroke Can Help Link Brain Regions to Speech Functions

Analysing the brains of stroke victims just days after the stroke allows researchers to link various speech functions to different parts of the brain, a breakthrough that may lead to better treatment and recovery, according to a study published in the journal Brain.

Tatiana Schnur, MD, Baylor College of Medicine, Houston, Texas, and colleagues evaluated the spontaneous language production of 65 patients who experienced a stroke by using storytelling. For the experiment, the patients were read the story of Cinderella and were then asked to retell it. The researchers used the Quantitative Production Analysis method and relied on 13 different measures for evaluation, including words per minute, types of words, and sentence length and formation.

They found that by evaluating patients between 1 and 13 days post-stroke, they were able to identify how different and critical components related to language production linked up with different regions of the brain. The researchers used cutting-edge techniques to relate the brain areas damaged in each individual to the degree of their impairment on these language-production measures. Specifically, they found that retrieving words and putting them into increasingly complex sentences relied on the left temporal and parietal lobes, while producing grammatical aspects of sentences relied on the left frontal lobe.

According to the authors, there are only a few other studies that have looked at patients with stroke in the acute stage, but those focused on ability to produce single words rather than providing a detailed analysis of language production. The majority of studies look at patients in the chronic stage of recovery, which is at least 6 months after the stroke. At that time, considerable reorganisation of language function in the brain may have occurred. Also, studying individuals at the acute stage allows for studying those with smaller areas of damage. Those with small lesions are likely to recover and thus not included in studies of chronic stroke, and examining these people allows for a more precise mapping between areas damaged and language abilities.

“Many patients in the chronic stage of stroke have significantly worse brain damage than acute patients and have plateaued with their recovery,” said co-author Randi Martin, Rice University, Houston, Texas. “Their brains cannot be evaluated in the same way as acute stroke patients.”

Future work will look at these same individuals at different stages during their first year of the recovery process. One important issue will be to determine what areas of brain damage and what language abilities will predict performance 1 year after stroke.

Martin hopes this work will help better understand how different brain regions recover from stroke. She expects the work will be useful in the design of treatment options for patients who have experienced a stroke, including early interventions that may boost long-term recovery.


Reference: https://academic.oup.com/brain/article/143/3/862/5802616

SOURCE: Rice University

Advances in neuroprosthetic management of foot drop: a review

Are you that fucking clueless that you think 'management' rather than curing foot drop is what survivors want?  OR DO YOU NOT CARE WHAT SURVIVORS WANT? Just whatever easy reviews you can do to get published? I'd have you all fired in a heartbeat.

Maybe after you are the 1 in 4 per WHO that has a stroke? Will that finally get you to do your job properly?

Advances in neuroprosthetic management of foot drop: a review

• Javier Gil-Castillo,
• Fady Alnajjar,
• Aikaterini Koutsou,
• Diego Torricelli &
• Juan C. Moreno 

Journal of NeuroEngineering and Rehabilitation volume 17, Article number: 46 (2020) Cite this article

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Abstract

This paper reviews the technological advances and clinical results obtained in the neuroprosthetic management of foot drop. Functional electrical stimulation has been widely applied owing to its corrective abilities in patients suffering from a stroke, multiple sclerosis, or spinal cord injury among other pathologies. This review aims at identifying the progress made in this area over the last two decades, addressing two main questions: What is the status of neuroprosthetic technology in terms of architecture, sensorization, and control algorithms?. What is the current evidence on its functional and clinical efficacy? The results reveal the importance of systems capable of self-adjustment and the need for closed-loop control systems to adequately modulate assistance in individual conditions. Other advanced strategies, such as combining variable and constant frequency pulses, could also play an important role in reducing fatigue and obtaining better therapeutic results. The field not only would benefit from a deeper understanding of the kinematic, kinetic and neuromuscular implications and effects of more promising assistance strategies, but also there is a clear lack of long-term clinical studies addressing the therapeutic potential of these systems. This review paper provides an overview of current system design and control architectures choices with regard to their clinical effectiveness. Shortcomings and recommendations for future directions are identified.(So your cop out is further research needed, rather than doing it yourself.)

Milk Fat Intake and Telomere Length in U.S. Women and Men: The Role of the Milk Fat Fraction

You'll need your doctor to analyze these 8 posts on dairy fat because they mostly come to the opposite conclusion about health benefits. I'm doing full fat milk, it tastes better. Did skim milk for decades prior to stroke.

• dairy fat (8)

 

Milk Fat Intake and Telomere Length in U.S. Women and Men: The Role of the Milk Fat Fraction

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Larry A. Tucker¹

¹Brigham Young University, College of Life Sciences, 106 SFH, Provo, Utah 84602, USA

Academic Editor: Ana Lloret

Received06 Jun 2019

Accepted04 Oct 2019

Published28 Oct 2019

Abstract

The associations between milk intake frequency and milk fat consumption and telomere length, an index of biological aging, were studied using an NHANES sample of 5,834 U.S. adults and a cross-sectional design. The milk consumption variables were assessed with the NHANES Diet Behavior and Nutrition questionnaire. The quantitative polymerase chain reaction method was used to measure leukocyte telomere length. Results showed that milk consumption frequency was not related to telomere length; however, there was a strong association between milk fat intake and telomere length. With the sample delimited to milk drinkers only, milk fat intake was linearly and inversely related to telomere length, after adjusting for the covariates (F=8.6,P=0.0066). For each 1 percentage point increase in milk fat consumed (e.g., 1% to 2%), adults had more than 4 years of additional biological aging. With milk fat intake divided into 5 categories (i.e., milk abstainers, nonfat, 1%, 2%, and full-fat milk), mean telomere lengths differed across the categories (F=4.1,P=0.0093  ). The mean telomere difference between the extremes of milk fat intake (nonfat vs. full-fat) was 145 base pairs, representing years of additional biological aging for full-fat milk consumers. Effect modification testing indicated that the milk fat and cellular aging association may be partly due to saturated fat intake differences across the milk fat groups. When the sample was delimited to adults reporting only high total saturated fat intake (tertile 3), the milk fat and telomere relationship was strong. However, when the sample was restricted to adults reporting only low saturated fat consumption (tertile 1), there was no relationship between milk fat intake and telomere length. Overall, the findings highlight an association of increased biological aging in U.S. adults who consumed high-fat milk. The results support the latest Dietary Guidelines for Americans (2015–2020), which recommend consumption of low-fat milk, but not high-fat milk, as part of a healthy diet.

1. Introduction

Investigations evaluating the effect of adult milk consumption on health and disease have produced inconsistent findings. Some studies indicate that the consumption of cow’s milk promotes health, while others show that it increases risk of disease and mortality. Numerous investigations highlight the mixed results.
In a 2018 study by Feskanich et al. [1], milk intake was associated with a lower risk of hip fracture, whereas in a 2018 investigation by Michaelsson et al., milk consumption was linked to an increased risk of hip fracture [2]. Further, a meta-analysis that included six studies focusing on women and three of men concluded that milk intake and hip fracture are unrelated [3].
In a meta-analysis of 19 studies concentrating on colorectal cancer, Aune et al. [4] determined that milk intake reduces risk, whereas in an evaluation of 32 investigations, the same researcher [5] concluded that milk consumption increases risk of prostate cancer. Similarly, some research indicates that dairy intake reduces the risk of type II diabetes [6, 7], whereas other studies show that dairy consumption is linked to increased insulin resistance [8–10]. Several investigations have concluded that dairy intake is unrelated to type II diabetes and associated metabolic factors [11, 12]. Lastly, in a Japanese cohort, milk intake was inversely associated with all-cause mortality [13], but in a Swedish group, milk consumption was related to increased all-cause mortality [14].
Clearly, the effects of adult milk consumption on health and disease are varied, and in recent years, questions about the influence of milk have been further complicated with debate about the effect of milk fat on disease risk. Is low-fat milk a healthier choice than full-fat? According to a 2017 study by Tognon et al., all-cause mortality is significantly higher among adults who consumed full-fat milk compared to medium- or low-fat milk [15]. Similarly, Talaei et al. found that Iranians who drink whole milk daily are at higher risk of all-cause mortality than their counterparts [16]. Likewise, whole milk intake is predictive of elevated prostate cancer mortality in studies by Lu et al. [17] and Song et al. [18]. Conversely, according to Crichton and Alkerwi, high intake of whole-fat dairy is inversely associated with obesity and abdominal adiposity compared to those with low consumption [19]. Additionally, research by Drehmer et al. shows that full-fat, but not low-fat, dairy is favorably related to the metabolic syndrome in adults [20].
The effects of milk and milk fat on cancer, heart disease, diabetes, and all-cause mortality have been reviewed extensively in the literature. With some investigations showing positive outcomes and others revealing negative, there remains much to learn about the effect of cow’s milk on health and disease in adults. The influence of milk fat, particularly low-fat compared to full-fat, also needs clarification.
To date, the influence of milk and milk fat on inflammation, oxidative stress, and cellular longevity has received little attention. Cellular longevity is often indexed objectively by measuring the length of telomeres [21, 22]. Adults with short telomeres tend to have more oxidative stress and chronic disease, including more heart disease, depression, obesity, and cancer, as well as earlier death, than their counterparts [23–25].
Telomeres add stability to and help safeguard chromosomes. Telomeres cap the ends of chromosomes with nucleoproteins. A simple analogy is that telomeres function like the caps that protect the end of shoe laces. Over time, as cells divide, telomeres become progressively and predictably shorter.
Although chronological age is the key factor accounting for the length of telomeres, other things contribute significantly. Research shows that oxidative stress is a critical factor [26, 27]. Moreover, lifestyle plays a major role. For instance, people who smoke have shorter telomeres than nonsmokers [28]. Adults with obesity have shorter telomeres than their counterparts [29], and inactive individuals have shorter telomeres than those who are physically active [30].
Biological aging is also affected by diet. Regular intake of healthy foods like nuts and seeds is associated with longer telomeres [31], whereas consumption of less healthy foods, like processed meats, is related to shorter telomeres [32]. Fiber intake goes hand-in-hand with longer telomeres [33], as does higher vegetable intake [34] and regular fruit consumption [35]. However, consumption of fats and oils is associated with shorter telomeres and increased biological aging [36, 37].
From a more physiological and molecular nutrition perspective, milk is a postnatal endocrine signaling system [38]. Milk consumption encourages mTORC1-mediated anabolism and growth. For example, extended full-fat cow’s milk consumption in mice increases energy intake and body weight and reduces insulin signaling in white adipose tissue compared to low-fat milk intake [39]. According to Melnik, to accomplish its mTORC1-activating role, four metabolic messengers are provided by milk: “1. essential branched-chain amino acids, 2. glutamine, 3. palmitic acid, and 4. bioactive exosomal microRNAs…” [38].
Research by Yasuda et al. indicates that unsaturated and saturated fatty acids have opposite effects on podocyte apoptosis by controlling mTORC1 activity via translocation onto lysosomal membranes [40]. Insulin and IGF-1 and essential branched-chain amino acids influence mTORC1 by activation of the kinase AKT pathway. Palmitic acid, the primary saturated fatty acid of milk fat globules, also activates mTORC1 at the lysosome [40]. In short, it appears that repeated mTORC1 activation contributes to endoplasmic reticulum stress, leading to premature aging and disease [38].
Although much is understood about diet, oxidative stress, and cellular longevity, the role of cow’s milk consumption, particularly milk fat, remains unclear. To date, the relationship between milk fat intake and telomere length has rarely been studied. Hence, the present study was conducted. Its purpose was to determine the extent cow’s milk consumption and the fat content of the milk account for differences in cellular aging, indexed using leukocyte telomere length in 5,834 women and men, representative of the U.S. adult population. A secondary objective was to assess the extent demographic, lifestyle, and other dietary factors influence the milk and telomere relationships. The role of saturated fat intake, a major part of the fat content of cow’s milk, was also a significant focus of the investigation.