Deans' stroke musings

Changing stroke rehab and research worldwide now.Time is Brain!Just think of all the trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 493 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:

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's quite disgusting that this information is not available from every stroke association and doctors group.
My back ground story is here:

Saturday, July 22, 2017

Determinants of Poststroke Fatigue among Stroke Survivors Undergoing Rehabilitation in Nigeria

I see no solution to fatigue presented. 50% of stroke survivors have fatigue. What the fuck are your doctors doing to cure that? Throwing up their hands and suggesting exercise?
To Cite : Vincent-Onabajo G, Adamu A. Determinants of Poststroke Fatigue among Stroke Survivors Undergoing Rehabilitation in Nigeria, Middle East J Rehabil Health Stud. Online ahead of Print ;In Press(In Press):e57478. doi: 10.5812/mejrh.57478.

The Automated Box and Blocks Test an Autonomous Assessment Method of Gross Manual Dexterity in Stroke Rehabilitation

Finally trying to do objective assessments of stroke rehab results.
  • Edwin Daniel Oña
  • Alberto Jardón
  • Carlos Balaguer
  • Edwin Daniel Oña
    • 1
  • Alberto Jardón
    • 1
  • Carlos Balaguer
    • 1
  1. 1.Robotics LabUniversity Carlos III of MadridLeganésSpain
Conference paper
Part of the Lecture Notes in Computer Science book series (LNCS, volume 10454)


Traditional motor assessment is carried out by clinicians using standard clinical tests in order to have objectivity in the evaluation, but this manual procedure is liable to the observer subjectivity. In this article, an automatic assessment system based on the Box and Blocks Test (BBT) of manual dexterity is presented. Also, the automatic test administration and the motor performance of the user is addressed. Through cameras RGB-D the execution of the test and the patient’s movements are monitored. Based on colour segmentation, the cubes displaced by the user are detected and the traditional scoring is automatically calculated. Furthermore, a pilot trial in a hospital environment was conducted, to compare the automatic system and its effectiveness with respect to the traditional one. The results support the use of automatic assessment methods of motor functionality, which in combination with robotic rehabilitation systems, could address an autonomous and objective rehabilitation process.

The efficacy of interactive, motion capture-based rehabilitation on functional outcomes in an inpatient stroke population: a randomized controlled trial

Cherry picking patients once again. A great stroke association president would ream these researchers out for leaving stroke survivors behind. All survivors deserve 100% recovery. Get them there you lazy fucking idiots.
First Published July 19, 2017 Research Article

To compare the efficacy of novel interactive, motion capture-rehabilitation software to usual care stroke rehabilitation on physical function.

Randomized controlled clinical trial.

Two subacute hospital rehabilitation units in Australia.

In all, 73 people less than six months after stroke with reduced mobility and clinician determined capacity to improve.

Both groups received functional retraining and individualized programs for up to an hour, on weekdays for 8–40 sessions (dose matched). For the intervention group, this individualized program used motivating virtual reality rehabilitation and novel gesture controlled interactive motion capture software. For usual care, the individualized program was delivered in a group class on one unit and by rehabilitation assistant 1:1 on the other.

Primary outcome was standing balance (functional reach). Secondary outcomes were lateral reach, step test, sitting balance, arm function, and walking.

Participants (mean 22 days post-stroke) attended mean 14 sessions. Both groups improved (mean (95% confidence interval)) on primary outcome functional reach (usual care 3.3 (0.6 to 5.9), intervention 4.1 (−3.0 to 5.0) cm) with no difference between groups (P = 0.69) on this or any secondary measures. No differences between the rehabilitation units were seen except in lateral reach (less affected side) (P = 0.04). No adverse events were recorded during therapy.

Interactive, motion capture rehabilitation for inpatients post stroke produced functional improvements that were similar to those achieved by usual care stroke rehabilitation, safely delivered by either a physical therapist or a rehabilitation assistant.

Inhibition of prolyl hydroxylases by dimethyloxaloylglycine after stroke reduces ischemic brain injury and requires hypoxia inducible factor-1α

Only 5.5 years old and I bet not one thing has been done to get this into a stroke protocol. No one cares about helping stroke survivors, certainly not the ASA, NSA or the WSO. You are completely on your own, start saving your money to hire your own researchers. Your children and grandchildren will need it.


Pathological oxygen deprivation inhibits prolyl hydroxylase (PHD) activity and stimulates a protective cellular oxygen-sensing response in part through the stabilization and activation of the Hypoxia Inducible Factor (HIF) 1α transcription factor. The present investigation tested the therapeutic potential of enhanced activation of oxygen-sensing pathways by competitive pharmacologic PHD inhibition after stroke, hypothesizing that post-ischemic PHD inhibition would reduce neuronal cell death and require the activation of HIF-1α. The PHD inhibitor dimethyloxaloylglycine (DMOG, 100 μM) reduced cell death by oxygen glucose deprivation (OGD), an in vitro model of ischemia, and the protection required HIF-1α. In vivo, DMOG (50 mg/kg, i.p.) administered 30 or 60 min after distal occlusion of the middle cerebral artery (MCA) in mice enhanced the activation of HIF-1α protein, enhanced transcription of the HIF-regulated genes vascular endothelial growth factor, erythropoietin, endothelial nitric oxide synthase, and pyruvate dehydrogenase kinase-1, reduced ischemic infarct volume and activation of the pro-apoptotic caspase-3 protein, reduced behavioral deficits after stroke, and reduced the loss of local blood flow in the MCA territory after stroke. Inhibition of HIF-1α in vivo by Digoxin or Acriflavine abrogated the infarct sparing properties of DMOG. These data suggest that supplemental activation of oxygen-sensing pathways after stroke may provide a clinically applicable intervention for the promotion of neurovascular cell survival after ischemia.


► PHD inhibition by DMOG after stroke reduces ischemic damage. ► Post-ischemic DMOG enhances peri-infarct HIF-1α expression. ► Neuroprotection by DMOG in vivo requires HIF-1α activity.


Focal cerebral ischemia
Hypoxia inducible factor
Prolyl hydroxylase

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ACRM Conference: Progress in Rehabilitation Research, Atlanta GA Oct. 23-28, 2017

I see nothing in the presentations that looks like protocols or anything to do with the neuronal cascade of death. Even worse, they went to the dark side and have speakers on Complementary Integrative Medicine.

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 schadenfreude hits the appropriate people.
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:

CMMC receives American Heart Association Award for quality stroke care - Lewiston, Maine

So fucking what!. 'Care' NOT results. Damn it all, do something for survivors, like get them to 100% recovery. You lazy blithering idiots, thinking 'care' is what survivors want.
Central Maine Medical Center has received the American Heart Association/American Stroke Association's Get With The Guidelines Stroke Gold Plus Quality Achievement Award.
The award recognizes the Lewiston hospital's commitment and success in ensuring stroke patients receive the most appropriate treatment according to nationally recognized, research-based guidelines based on the latest scientific evidence.
To receive the Gold Plus Quality Achievement Award, hospitals must achieve 85% or higher adherence to all Get With The Guidelines stroke achievement indicators for two or more consecutive 12-month periods and also achieve 75% or higher compliance with five of eight stroke quality measures.
These quality measures are designed to help hospital teams provide the most up-to-date, evidence-based guidelines with the goal of speeding recovery and reducing death and disability for stroke patients. They focus on appropriate use of guideline-based care for stroke patients, including aggressive use of medications such as clot-busting and anti-clotting drugs, blood thinners and cholesterol-reducing drugs, preventive action for deep vein thrombosis and smoking cessation counseling.
"A stroke patient loses 1.9 million neurons each minute stroke treatment is delayed. This recognition further demonstrates our commitment to delivering advanced stroke treatments to patients quickly and safely," Dr. Peter Tilney, CMMC Emergency Department co-medical director, said in a news release.
Tilney said the recognition from the American Heart Association and American Stroke Association "further reinforces our team's hard work."
Dr. Paul Heidenreich, national chairman of the Get With The Guidelines Steering Committee and professor of Medicine at Stanford University, said research shows that hospitals adopting the Get With The Guidelines program Research are working to align patient care with the latest research-based guidelines for stroke care.

Friday, July 21, 2017

How I fail at being disabled - TED talk

A TED talk. I'm also failing at this, because I don't consider myself disabled. I do anything I want to do regardless of the consequences.

View the Program for the 2017 Canadian Stroke Congress.

Ask your doctor what rehabilitation protocols come out of this.
View the Program for the 2017 Canadian Stroke Congress.

Agent clears toxic proteins and improves cognition in neurodegeneration models - Alzheimers/Parkinsons

You might need this, so start training your doctor right now on this possibility.
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.

Parkinson’s Disease May Have Link to Stroke

Georgetown University Medical Center
LONDON -- Researchers have found cell receptors abnormally overexpressed in post-mortem brains of those with Parkinson's and Alzheimer's diseases, and that they can be inhibited in animal models to clear toxic protein buildup, reduce brain inflammation, and improve cognitive performance.
These dual findings, presented by Georgetown University Medical Center (GUMC) researchers at the Alzheimer's Association International Conference in London, mark the first time that the receptors, discoindin domain receptors (DDRs), have been understood to play a role in Parkinson's and Alzheimer's diseases. (They are primarily known as potential targets against cancer.)
"Activation of these cell receptors appear to prevent brain cells from cleaning out the trash -- the toxic buildup of proteins, such as alpha-synuclein, tau and amyloid, common in neurodegenerative diseases," says the study's senior author, Charbel Moussa, MBBS, PhD, director of Georgetown's Laboratory for Dementia and Parkinsonism, and scientific and clinical research director of the GUMC Translational Neurotherapeutics Program.
When DDRs are over-expressed, their actions become destructive. One reason may be that DDRs are protein enzymes known as tyrosine kinases that act as on and off switches of the cell self-cleaning process known as autophagy. Excess DDRs activation may switch off autophagy, resulting in build-up of toxic proteins inside brain cells and possibly breakdown of the blood-brain barrier, common in neurodegenerative diseases, he says.
DDRs inhibition with a tyrosine kinase inhibitor appears to insulate the brain via blood-brain barrier repair, which prevents harmful immune cells that circulate in the body from getting into the brain where they can indiscriminately attack and kill healthy and sick neurons, like those that have been unable to perform autophagy to "take out their trash," says Moussa.
"We studied an experimental tyrosine kinase inhibitor that enters the brain and inhibits DDRs," explains Moussa, associate professor of neurology. "Inhibition of these receptors with a low dose of the agent, LCB-03-110, or reduction of DDRs expression in several models of Parkinson's and Alzheimer's disease, allows nerve cells to switch on autophagy to clear toxic proteins and help the brain insulate itself from circulating inflammatory cells. This led to cognitive improvement in our animal models."
Moussa has found other agents that target the process of autophagy. One such agent nilotinib (Tasigna® by Novartis), used to treat leukemia, is being studied in patients with Parkinson's and Alzheimer's diseases.
Study collaborators include, from Moussa's lab Michaeline Hebron, MS, Monica Javidnia, and Irina Lonskaya, PhD, a postdoctoral researcher.
Georgetown has filed a patent application related to use of certain DDR inhibitors for the treatment of neurodegenerative diseases. Moussa is the named inventor of the intellectual property protected. Also, Georgetown holds an issued US patent on related technology for the use of nilotinib for the treatment of certain neurodegenerative diseases and has other pending patent applications in US and foreign jurisdictions. Moussa is also the named inventor on this related intellectual property, which the university has licensed to a company for further development and commercialization.

Stressful experiences can age brain 'by years', Alzheimer's experts hear

Does this explain your aged/lost 5 years of your brain due to your stroke due to the stress of your doctor not knowing one damn thing about getting you 100% recovered?
Child’s death, divorce or job loss linked to poorer cognition in later life, study finds, with African Americans more susceptible.
Stressful life experiences can age the brain by several years, new research suggests. Experts led by a team from Wisconsin University’s school of medicine and public health in the US found that even one major stressful event early in life may have an impact on later brain health.
The team examined data for 1,320 people who reported stressful experiences over their lifetime and underwent tests in areas such as thinking and memory. The subjects’ average age was 58 and included 1,232 white Americans and 82 African Americans. A series of neuropsychological tests examined several areas, including four memory scores (immediate memory, verbal learning and memory, visual learning and memory, and story recall).
Stressful life experiences included things such as losing a job, the death of a child, divorce or growing up with a parent who abused alcohol or drugs. The results showed that a larger number of stressful events was linked to poorer cognitive function in later life.
When looking specifically at African Americans, the team found they experienced 60% more stressful events than white people during their lifetimes. Researchers said that, in African Americans, each stressful experience was equivalent to approximately four years of cognitive ageing.
The study, which has not been published in a peer-reviewed journal, was presented at the Alzheimer’s Association international conference in London.
Dr Maria Carrillo, the chief science officer for the Alzheimer’s Association, said: “The stressful events that the researchers were focusing on were a large variety ... the death of a parent, abuse, loss of a job, loss of a home ... poverty, living in a disadvantaged neighbourhood, divorce.” She said that even a change of school could be regarded as a stressful life event for some children.
Dr Doug Brown, the director of research at the Alzheimer’s Society, said: “We know that prolonged stress can have an impact on our health, so it’s no surprise that this study indicates stressful life events may also affect our memory and thinking abilities later in life. However, it remains to be established whether these stressful life events can lead to an increased risk of dementia.
“Studying the role of stress is complex. It is hard to separate from other conditions such as anxiety and depression, which are also thought to contribute towards dementia risk.

“However, the findings do indicate that more should be done to support people from disadvantaged communities that are more likely to experience stressful life events. As we improve our understanding of risk factors for dementia, it is increasingly important to establish the role that stress and stressful life events play.”
Other research has suggested there are plausible links between stress and chronic inflammation, which in turn may accelerate the development of dementia. But experts believe that a health lifestyle and a healthy diet can help mitigate this risk, even for those people going through stressful events.

Coffee with Viagra-like ingredient recalled after FDA discovery

Too bad, Both coffee and viagra are great stroke rehab and dementia prevention possibilities.
Don't do this on your own, but see the possibilities of Viagra here:

16 posts on Viagra here.

139 posts on coffee here. 

No drinking of coffee without your doctors prescription.
Albert Yee said the coffee is everywhere you look in the densely packed vendor stalls along avenues in Malaysian cities: an instant mix with a natural ingredient similar to what's found in Viagra that helps men with erectile dysfunction. And Yee wanted a piece of the action.
“There are whole streets of it, like tequila in Mexico,” Yee told The Washington Post by phone Thursday, describing how his one-man Texas import business is now at the center of a nationwide voluntary recall coordinated by the U.S. Food and Drug Administration.
The FDA announced last week that Yee's company, Grand Prairie, Tex.-based Bestherbs Coffee LLC, is voluntarily recalling all lots of the uniquely spelled “New of Kopi Jantan Tradisional Natural Herbs Coffee” due to undeclared ingredients, including desmethyl carbodenafil and milk, sold between July 2014 and June 2016.
“Desmethyl carbodenafil is structurally similar to sildenafil, the active ingredient in Viagra, an FDA-approved prescription drug for erectile dysfunction,” the FDA said in a statement.
The “undeclared ingredient may interact with nitrates found in some prescription drugs, such as nitroglycerin, and may lower blood pressure to dangerous levels,” the FDA noted.

“Men with diabetes, high blood pressure, high cholesterol or heart disease often take nitrates,” the FDA said. It also warned that the coffee's unlisted milk ingredient could be dangerous for people with allergies or sensitivities to milk.
Both the FDA and Yee said there have been no consumer health issues related to his company's coffee.
Yee said he was not sure how much coffee was involved in the recall, but estimates he'll receive a few hundred to a thousand bags from customers that he will then hand over to the FDA for destruction.
It will be the FDA's latest recall involving coffee laced with the ingredient. Stiff Bull Herbal Coffee faced a similar recall last year, as did the sellers of Caverlo Natural Herbal Coffee in May.
In both instances, the sellers advertised the inclusion of Tongkat Ali, the root of a tree found in Malaysian rain forests and distilled to pill form, or concentrated and mixed with coffee or tea. In 2014, ABC News sent a reporter into the bush to scout for the root, which can only be extracted with tools to partially topple the tree, making the root particularly difficult to harvest for mass production.
The producers of Stiff Bull Herbal Coffee claimed the coffee sellers mixed in desmethyl carbodenafil to cut down on high costs of the root, raising the possibility the same thing happened with Yee's coffee.
Ong Boon Kean, a senior researcher at the Forest Research Institute of Malaysia, told ABC that Tongkat Ali can boost low testosterone and sperm count.
Yee said the recall has made his next business decision easy.
“I'm 67,” he said. “I'm going to retire.”

Restoring auditory cortex plasticity in adult mice by restricting thalamic adenosine signaling

I would expect human testing to begin almost immediately. We need neuroplasticity up the wazoo since no one yet knows how to make neuroplasticity repeatable on demand. Of course that will never occur since we have NO stroke leadership and NO stroke strategy.

+ See all authors and affiliations
Science  30 Jun 2017:
Vol. 356, Issue 6345, pp. 1352-1356
DOI: 10.1126/science.aaf4612
You are currently viewing the abstract.
View Full Text


Circuits in the auditory cortex are highly susceptible to acoustic influences during an early postnatal critical period. The auditory cortex selectively expands neural representations of enriched acoustic stimuli, a process important for human language acquisition. Adults lack this plasticity. Here we show in the murine auditory cortex that juvenile plasticity can be reestablished in adulthood if acoustic stimuli are paired with disruption of ecto-5′-nucleotidase–dependent adenosine production or A1–adenosine receptor signaling in the auditory thalamus. This plasticity occurs at the level of cortical maps and individual neurons in the auditory cortex of awake adult mice and is associated with long-term improvement of tone-discrimination abilities. We conclude that, in adult mice, disrupting adenosine signaling in the thalamus rejuvenates plasticity in the auditory cortex and improves auditory perception.

Behaviorally Selective Engagement of Short-Latency Effector Pathways by Motor Cortex

What about humans?  If the motor cortex is not needed for walking in mice then why is my walking still screwed up?  Of course my pre-motor cortex is mostly dead also, no idea how much white matter damage there is underlying those cortex areas. Because I never got any objective damage diagnosis I have no idea what needs fixing.
Publication stage: In Press Corrected Proof


  • In mice, motor cortex is required for a trained forelimb task, but not walking
  • Motor cortex activates short-latency effector pathways only during the trained task
  • Distinct weighted sums of motor cortical firing patterns vary strongly in each task
  • This change could permit motor cortex to engage short-latency pathways differentially


Blocking motor cortical output with lesions or pharmacological inactivation has identified movements that require motor cortex. Yet, when and how motor cortex influences muscle activity during movement execution remains unresolved. We addressed this ambiguity using measurement and perturbation of motor cortical activity together with electromyography in mice during two forelimb movements that differ in their requirement for cortical involvement. Rapid optogenetic silencing and electrical stimulation indicated that short-latency pathways linking motor cortex with spinal motor neurons are selectively activated during one behavior. Analysis of motor cortical activity revealed a dramatic change between behaviors in the coordination of firing patterns across neurons that could account for this differential influence. Thus, our results suggest that changes in motor cortical output patterns enable a behaviorally selective engagement of short-latency effector pathways. The model of motor cortical influence implied by our findings helps reconcile previous observations on the function of motor cortex.

Greater gait with gravity

It is in the neurorehabilitation section of Science, but no visible extract. So send your doctors after it. Everything in stroke research should be publicly available through our fucking failures of stroke associations. But they can't even do that one little thing for survivors.

Thursday, July 20, 2017

Fine motor skills are often impacted by stroke. Try these exercises to help improve strength and dexterity.

They assume high functionality already if you can even attempt these.  I'm sure these were done by normal people, not stroke survivors. With 30% of survivors having spastiscity none of those could keep fingers straight as shown in the pictures. Good conscience laundering to make the American Stroke Association feel like they are doing something. What a crock.

A multicentre study of how goal-setting is practised during inpatient stroke rehabilitation

Totally fucking useless, The goals were biased by the therapists and doctors. Survivors want 100%  recovery. So get them there.
First Published July 17, 2017 Research Article

To describe goal-setting during inpatient stroke rehabilitation.

There were two stages: an electronic questionnaire for multidisciplinary teams and an analysis of goal-setting documentation for rehabilitation patients.

Five inpatient stroke units.

Staff involved in goal-setting and patients undergoing stroke rehabilitation.

A total of 13 therapists and 49 patients were recruited, and 351 documented goals were examined. All units used therapist-led goal-setting (60% of goals were set by therapists). In total, 72% of goals were patient-focused but patients and families were rarely directly involved. Goals focussed on basic mobility and activities of daily living (~50% and ~25% of goals, respectively). Only 41% of documented goals met the SMART criteria. Review of progress was limited: 48% of goals were never reviewed and 24% of the remainder were merely marked as ‘ongoing’ without a date or plan for completion. New goals and actions were often documented without any connection to previous goals. Integration between goals and treatment/action plans was mixed. In two units, goals were unconnected to a treatment or action plan, but for the remainder it was 90%–100%. However, that connection was generally vague and amounted to suggestions of the type of treatment modality that staff might employ.

Goal-setting during inpatient stroke rehabilitation is therapist-led but discussed with the multidisciplinary team. Therapists mainly identified patient-focussed mobility and activities of daily living goals. Monitoring progress and revising goals were often uncompleted. Links between goals and treatment, action plans and progress were patchy.

Startup touts neuro-stimulation as 'medicine for the brain'

Sounds like a lot of 'woo' to me. 'Latent potential' sounds like the discredited, 'You only use 10% of your brain'.
They look like a set of fancy headphones.
But a set of spikes inside the band act as electrodes to stimulate the brain.
According to California startup Halo Neuroscience, the device can help improve the performance of athletes, pilots and surgeons, and potentially help rehabilitation for stroke victims.

"The brain is an electrical organ," said Daniel Chao, a physician and co-founder of Halo, in discussing the product at this week's Fortune Brainstorm Tech conference.
By stimulating the motor cortex, Chao says the Halo device can "extract latent potential" in the brain to improve performance for people who rely on making quick decisions on movements such as athletes.
"We think of athleticism athletes, pilots as athletes."
Halo, which has raised some $10 million in funding, began selling the Halo Sport device last year for $749.
The San Francisco startup has also concluded deals with the San Francisco Giants baseball team and the U.S. Olympic ski team to integrate Halo in training programs.
Chao said the U.S. military is the company's largest customer, aiming to help improve the performance of special operations team
Users are advised to wear the headset for 20 minutes a day, to get electrical stimulation "to build stronger, more optimized connections between your brain and muscles," according to the company website.
Chao, who trained as a doctor and studied neuroscience at Stanford, previously worked at a startup called Neuro Pace which uses electrical stimulation to treat epilepsy.
He said his research found little help from drugs for the disease and decided to study "electricity as medicine for the brain."
Chao said he hopes to obtain U.S. government approval to use the technology for medical applications.
"As a doctor I want to see this achieve an FDA (Food and Drug Administration) approval," he told the conference. "The first application could be for stroke rehab."

One-third of dementia cases could be prevented, report says

More useless generalized crap. This is just conscience laundering and a way to blame the patient for getting dementia. 'We told you about these lifestyle factors when you were 15 years old'. 'You obviously didn't listen and since you didn't listen, that is a pre-existing condition and insurance will pay for nothing in your dementia care'. You're screwed.
Maybe my ideas here?

Dementia prevention 19 ways
One-third of cases of dementia worldwide could potentially be prevented through better management of lifestyle factors such as smoking, hypertension, depression, and hearing loss over the course of a lifetime, according to a new report.
Across the globe, about 47 million people were living with Alzheimer's and other forms of dementia in 2015. That number is projected to triple by the year 2050 as the population ages. Health care costs associated with dementia are enormous, with an estimated $818 billion price tag in 2015.
The new study, published in The Lancet and conducted by the first Lancet Commission on Dementia Prevention and Care, brought together 24 international experts to review existing dementia research and provide recommendations for treating and preventing the devastating condition.
"Dementia is the greatest global challenge for health and social care in the 21st century," lead study author Professor Gill Livingston, of University College London, told CBS News. "The purpose of the commission was therefore to address it by consolidating the huge strides and emerging knowledge as to what we should do to prevent dementia and intervene and care for people with dementia."
There is currently no drug treatment to prevent or cure dementia. But the report highlights the impact of non-drug interventions and identifies nine modifiable risk factors through various stages of life — beginning in childhood — that affect the likelihood of developing dementia.
To reduce the risk, factors that make a difference include getting an education (staying in school until over the age of 15); reducing high blood pressure, obesity and diabetes; avoiding or treating hearing loss in mid-life; not smoking; getting physical exercise; and reducing depression and social isolation later in life. About 35 percent of dementia cases are attributable to these factors, the analysis found. Removing them could then theoretically prevent 1 in 3 cases.
In contrast, finding a way to target the major genetic risk factor, a gene called the apolipoprotein E (ApoE) ε4 allele, would prevent less than 1 in 10 cases – or about 7 percent.
"There's been a great deal of focus on developing medicines to prevent dementia, including Alzheimer's disease," commission member Lon Schneider, M.D., a professor of psychiatry and the behavioral sciences at the Keck School of Medicine of USC, said in a statement. "But we can't lose sight of the real major advances we've already made in treating dementia, including preventive approaches." Schneider presented the findings at the Alzheimer's Association International Conference (AAIC) 2017.
Of the nine risk factors, the researchers identified the three most common ones that could be targeted for dementia prevention.
The first is increasing education in early life, which the report estimated could reduce the total number of dementia cases by 8 percent if all people worldwide continued their education until over the age of 15.
The researchers note that not completing secondary education could raise dementia risk by reducing what's referred to as "cognitive reserve." It's believed that education and other mentally stimulating tasks help the brain strengthen its networks so it can continue to function at a higher level even if it starts to decline later in life.
For the first time, the researchers also identified hearing loss as a major modifiable risk factor for dementia. They estimated that reducing hearing loss in mid-life could also reduce the number of dementia cases by 9 percent if all people were treated.
Livingston notes that research surrounding hearing loss and dementia is still in early stages and the link likely has something to do with the social isolation that can come with losing the ability to hear.
"They may work in similar ways as they reduce the chance of interactions and conversations, which are like exercise for the brain and enrich it and predispose to depression," she said.
It's not clear from medical research yet whether using hearing aids can counteract this risk.
Additionally, the researchers found the number of dementia cases worldwide could be reduced by 5 percent if all people stopped smoking. It's particularly important to stop smoking later in life, they say, to reduce neurotoxins and improve heart health, which in turn improves brain health.
Other interventions likely to reduce dementia rates include increased physical activity and treating high blood pressure and diabetes.
The study authors say the report can offer guidance on ways to reduce the risk of dementia throughout life and improve the care for those living with the disease.
"This includes providing safe and effective social and health care interventions in order to integrate people with dementia within their communities," Schneider said. "Hopefully this will also ensure that people with dementia, their families and caregivers, encounter a society that accepts and supports them."
It's important to note that lifestyle interventions will not delay or prevent all dementia cases. But the researchers say they are hopeful that the report will help shift more focus to concrete steps that can be taken to help avoid the disease.
"We hope that this report will feed into individual nations' dementia policies and public health strategies, be used by individual clinicians to inform and improve their practice, and through media publicity inform the general public of what they can do to help avoid dementia, which is the most feared illness in old age."