A longevity researcher says everyone's too obsessed with living forever. Here are his 2 anti-aging habits instead.

 I can do the restricted eating, I'm close with only 1 meal a day. Heavy exercise; NO, because my doctor and therapists COMPLETELY FAILED AT GETTING ME 100% RECOVERED!

My doctor assumed NO RESPONSIBILITY for my recovery by writing three prescriptions of E.T.(Evaluate and Treat) to my OT, PT and ST! If yours does that; fire them immediately and get them fired for incompetence! I could easily train a chimpanzee for that task.

A longevity researcher says everyone's too obsessed with living forever. Here are his 2 anti-aging habits instead.

• Dr. Steven Austad is the scientific director of the American Federation for Aging Research.
• Austad believes too many people are obsessed with longevity, focusing on dubious trends.
• Austad follows 2 habits for his health: heavy exercise and time-restricted eating.

Dr. Steven Austad, the scientific director of a nonprofit researching healthy aging, never fretted too deeply about his own longevity.

"I used to train lions for a living," Austad told Business Insider. "It was not something that you would do if you were thinking about living a long time."

Prior to his career at the American Federation for Aging Research, Austad was a biologist who focused on field work in places like Venezuela and East Africa. He became interested in aging research not because he wanted to crack the code to living forever, but to learn why healthy cells age at all. When he entered the field, he said many researchers had the same question, and were not necessarily motivated by extending their own lifespans.

Things have changed since, as more people pursue anti-aging trends — often, Austad said, with dubious science backing the claims. "I'm not one of those people who spends an hour a day in a hyperbaric chamber or gets infusions of some weird protein-vitamin cocktail," he said. "But in fact, I'm quite healthy, despite the years I spent in the field, and I had malaria."

For example, Austad doesn't take supplements, citing a lack of strong-enough evidence of their guaranteed longevity benefits, and he enjoys a glass of wine here and there. "If you spend all your time thinking about how long you're going to live, you kind of forget to live," he said.

Related video: Arnold Schwarzenegger's 5 daily habits that could add years to your life (Bodybuilding Bros)Austad shared a few simple longevity habits he's followed for years, which he said are both science-backed and "basically the things that my mother probably told me."

He exhausts himself at the gym

When Austad was a field biologist, he traveled to Papua New Guinea. Upon landing, his group had to climb to the top of a mountain. The village headman gave Austad's bag to his 12-year-old daughter to carry, because Austad would "slow them down too much." Offended at first, Austad was grateful to be baggage-free an hour later. He was also stunned by the girl's level of fitness.

"To me, that was a window into what our bodies evolved to be like," he said. The villagers never had osteoporosis or other conditions caused by sedentary lifestyles.

It's a huge reason he prioritizes serious exercise almost every day of the week.

"I am kind of a gym rat," Austad said. Because of an old lion injury on his knee, he bikes for his cardio, ranging from 40 minutes to an hour and a half. He also prioritizes strength training, alternating areas of his body and always including some core exercises.

Research shows many benefits of exercise. "It used to be that we thought this exercise good for your heart and lungs, good for your muscles, keeping your bones strong," Austad said. "Now we know there are cognitive benefits, there are immune benefits, there are all kinds of benefits that we never appreciated."

One of the biggest ones for him is quality sleep, so much so that he sets strict boundaries around his workout time. "I don't have great sleep unless I physically exhaust myself, and I just figure I have to live with that."

He only eats twice a day

Austad was practicing time-restricted eating, a form of intermittent fasting, before it became trendy in the longevity space. It felt like his "natural rhythm" to eat a late breakfast around 11 a.m., skip lunch, and finish the day with dinner around 6 or 7 p.m.

"Now, recently it's come out that there are all kinds of health benefits associated with that kind of timing, and I'm kind of embarrassed that I didn't appreciate that earlier," he said.

Intermittent fasting schedules vary and can potentially be risky, according to some studies. Austad's schedule aligns with his circadian rhythm, which researchers believe can improve metabolic health.

He recalled speaking at a calorie restriction conference and attending the banquet after. "It was basically leaves and nuts and zero-calorie dressing," he said. "Even if it made you healthier, and I'm not convinced that it does, it's just too much for me."

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WSO(World Stroke Organization) Key advocacy priorities

Their #5 takes NO RESPONSIBILITY upon themselves to actually solve stroke; 100% recovery for all!  In my opinion the WSO is completely fucking worthless to survivors, they do nothing, they will never do anything!

WSO(World Stroke Organization) Key advocacy priorities

 Stroke is gaining ground globally – over the past 10 years the lifetime risk of stroke in adults over 25 has risen from 1 in 6 to 1 in 4. Over 100 million people in the world have experienced stroke and projections for the next decades suggest that this number will increase strongly. The global cost of stroke looks set to hit US$1 trillion. It is clear that the long-term personal and socioeconomic impact of stroke requires specific policy and action. WSO has identified five advocacy priorities to drive the development and implementation of evidence-based policy stroke.

1 Stroke prevention - reducing exposure to stroke risk factors; implementing and promoting motivational mobile technologies; facilitating access to low dose combination medications in one polypill for specific groups and investing in the training and deployment of community health workers. 

2 Stroke recognition – improving public awareness of the signs of stroke and the benefits of timely access to quality acute stroke care.(NOT RESULTS OR RECOVERY!)

3 Stroke services – ensuring context-specific implementation of its Global Stroke Services Guideline and Action Plan(NOT PROTOCOLS!) and its companion WSO Roadmap to Delivering Quality Stroke Care throughout the world. 

4 Life after stroke - ensuring people affected by stroke have access to neuro-rehabilitation units and when needed to long-term rehabilitation and support that is essential for health, well-being and social participation. WSO invests in and advocates for the meaningful involvement of stroke survivors and caregivers in the development of national, regional and global policy. (No you don't, you have zero outreach to survivors. Quit your fucking lying!) 

5 Action and accountability – WSO calls for bolder actions from both governmental and non-governmental organisations, including taxation from sugar loaded drinks, tobacco and alcohol (STAX) towards improving stroke treatment, prevention and rehabilitation services and to enhance population-based prevention programmes. WSO supports and advocates for the development and delivery of evidence-based comprehensive measures that encompass prevention, acute care, rehabilitation and support. 

 A bunch of bleating videos at the link. TLDW(Too long, didn't watch)

A social dimension for brain health: the mounting pressure

 

You can obviously see that the WSO has zero interest in stroke survivors. And they take no responsibility in solving stroke, pushing prevention only.

A social dimension for brain health: the mounting preessure

• The Lancet Neurologysolving strokerevet

Published:October, 2021DOI:https://doi.org/10.1016/S1474-4422(21)00295-7 o

The prevention of stroke and dementia is the title and focus of the first webinar in an ongoing series on Global Policy organised by the World Stroke Organization (WSO). The series follows up on the WSO Declaration from 2020 that recommended “a joint prevention strategy” for these neurological diseases “given the commonality of risk factors and the reciprocal relationship of stroke and dementia”. WSO wants population-wide primary prevention strategies to become a global priority, which is a sound evidence-based approach to stop the huge burden of these diseases. However, implementation of population-wide strategies cannot be done in neurology clinics and, instead, requires emphasis on improving public health.

The burden of stroke keeps increasing, particularly in low-income countries. The diverging trends between high-income countries (in which some decreases in stroke-related mortality and disability have been accomplished) and other regions are growing. Underlying these disparities are both the limited availability and quality of stroke services in low-income and middle-income countries and also the mounting exposure of their citizens to some modifiable risk factors. Among such factors, globally, high systolic blood pressure is associated with the highest number of disability-adjusted life-years (DALYs) after a stroke. More than 50% of stroke-related DALYs in low-income countries can be attributed to hypertension.

This situation is not surprising. The high risk of cardiovascular events and stroke attributable to hypertension has been well known by epidemiologists for decades. Nevertheless, the number of people with hypertension has doubled over the past 30 years. In 2019, more than half of them (about 720 million people) were not receiving any treatment and were possibly unaware of their condition. Although in several high-income countries the prevalence of hypertension has decreased substantially, in poorer countries the rates keep increasing.

Hypertension, particularly in midlife, is also associated with an accelerated rate of cognitive decline at older age and accounts for a substantial proportion of dementia cases worldwide. Several studies have demonstrated that blood pressure lowering can reduce the progression of vascular lesions in the brain (ie, the volume of white matter hyperintensities, which is a risk factor for cognitive impairment). Furthermore, the US and Puerto Rico Systolic Blood Pressure Intervention Trial (SPRINT) also showed that intensive blood pressure control (<120 mm Hg) can reduce the incidence of not only stroke and cardiovascular events, but also mild cognitive impairment. Findings from these and several other trials and longitudinal studies support blood-pressure control as an intervention for the primary prevention of dementia. Evidence is not yet conclusive, however, with respect to optimal blood pressure thresholds and timing for blood pressure control, or regarding the population that could benefit the most. Further research is needed to determine these parameters. In the meantime, while optimal management and use of antihypertensive drugs are being outlined, the strategies for primary prevention of dementia must address inequalities in exposure to hypertension and other risk factors.

The reduction of a risk factor responsible for such an enormous burden of stroke and dementia is indeed a public-health challenge that requires societal action. For instance, policies should make healthy diets with reduced salt intake, and more fruits and vegetables, affordable and widely available. In low-income countries, primary care and universal health coverage are key to improve detection and monitoring of hypertension. Better socioeconomic status leads to a longer, healthier life and more resilient brain. Incidence rates of stroke and dementia are now lower in many high-income countries than they were a few decades ago because of better living conditions and improved access to healthcare and education throughout the lifespan.

In their Declaration for a common prevention strategy for stroke and dementia, WSO rightly calls for “abandoning categorisation of people into low, moderate, and high risk” and promoting instead a “holistic prevention approach” for the whole population. Such an approach must have a life-course perspective of brain health, starting in early life, with favourable environments that facilitate healthy diets, physical activity, and better education. Hypertension control and the consequent prevention of neurological disease will be achieved only by considering the many non-medical factors that influence neurological outcomes.

Further reading on social determinants of health: Hilal S, Brayne C. Epidemiologic Trends, Social Determinants and Brain Health: time to address the blind spots of life course inequalities. Stroke 2021 (in press)

 

How to Relax a Clenched Hand After Stroke Using Progressive Treatment from Flint Rehab

You will notice in there that there is zero responsibilty for your doctor and therapists to get you recovered. NO PROTOCOLS. You are pretty much completely on your own.

How to Relax a Clenched Hand After Stroke Using Progressive Treatment from Flint Rehab

What It Means When They Say “Every Stroke Is Different” from Flint Rehab

I ABSOLUTELY HATE THIS FUCKING LAZY RESPONSE, IT LETS YOUR STROKE TEAM OFF THE HOOK WHEN THEY REALLY SHOULD BE WALKING THE PLANK FOR INCOMPETENCE. This chaps my ass!  Notice the shift in responsibility here, your doctor and therapist are responsible for NOTHING!

What It Means When They Say “Every Stroke Is Different” from Flint Rehab

Questions about recovery after stroke often elicit a common response from medical teams: “Every stroke is different, so every recovery will be different.” But what exactly does that mean?
You’re about to discover two reasons why every stroke is different. This information should help you ask better questions when consulting your doctor or therapist.
To get started, it helps to look at the location of the stroke.

Location, Location, Location

A stroke occurs when the supply of blood to an area of the brain becomes compromised. Until the stroke is treated, the lack of oxygen-rich blood results in damage to the local brain tissue.
A stroke can occur anywhere within the brain, so different functions will be affected. No stroke is the same. The side effects that occur will fluctuate from person to person based on where the stroke occurred and what functions that area of the brain controlled.
For instance, a stroke that occurs in the temporal lobe will create different side effects than a stroke in the parietal lobe, because each area of the brain controls different functions.
The area of the brain affected by stroke provides a strong clue about which stroke side effects may occur.
However, even an expert on brain anatomy will have difficulty predicting the outcomes of a single stroke because every brain is wired a bit differently.

Brain Anatomy: Why Every Stroke Is Different

The brain is a large, complex organ. Each area of the brain controls different functions. For instance, one area controls language while a separate area controls arithmetic.
However, every brain is wired a bit differently, sometimes even drastically.
For example, the language center of the brain is generally understood to be located in the left hemisphere. This is why left hemisphere strokes often result in language difficulties like aphasia.
However, in some people that are left-handed, the language center is located on the opposite side, in the right hemisphere. This means that a left hemisphere stroke could leave language skills unaffected if the person is left-handed.
As you can see, every brain is different, which inevitably means that every stroke is different too. Still, every patient should ask about the location of the stroke, as it can still provide useful insight.
Although nothing is clear-cut, the good news is that, no matter how your brain is organized or where the stroke occurred, recovery is possible.

How the Brain Is Capable of Changing Itself

Did you know that the brain can “bounce back” from injury like stroke through its own self-healing?
Not too long ago, experts thought that the brain was incapable of change beyond the childhood years. Scientists used to claim that brain anatomy was fixed, and that the brain would only enter a state of slow deterioration after the formative childhood years.
This myth has since been dubunked. An excellent book on this subject is The Brain That Changes Itself by Norman Doidge, MD — it’s one of our top recommended books for stroke recovery.
Thanks to medical researchers like Doidge, we are now aware that the human brain is immensely capable of change. Not only is it constantly adapting and reorganizing itself throughout your entire life, but the brain can also bounce back from injury like stroke.
The process of the brain changing itself is called neuroplasticity. This is how stroke survivors can bounce back after their injury.
Neuroplasticity allows functions that were once located in the damaged areas to be “wired over” to healthy areas of the brain. This is how rehabilitation aims to help stroke patients recover.
It requires immense effort on the patient’s behalf, because the brain needs constant reinforcement to reorganize itself. However, stroke survivors have a chance at regaining lost skills with enough time, practice, and diligence.

Taking Charge of Your Recovery(Notice, NOTHING FOR YOUR DOCTOR OR THERAPIST TO DO!)

The phrase “every stroke is different” has gained popularity due to the vast nuances in the size and location of stroke, along with the differences in brain organization across the population.
This means that understanding the area of the brain affected by stroke provides a strong clue about the side effects that may occur. However, it’s not a definitive answer. Instead, stroke patients should pursue highly individualized paths to recovery.
Although the ambiguities can be frustrating, patients should find hope in the brain’s innate and miraculous ability to bounce back from stroke and reorganize itself based on your hard work.(NOT YOUR DOCTOR OR THERAPIST!)

Mental imagery to win an Olympic medal

From the New Scientist issue of February 2016. 

'Take the British athlete Steve Backley, a bronze medalist in the javelin at the 1992 Barcelona Olympic Games, who sprained his ankle just before the 1996 Atlanta games. He was on crutches for weeks, so he trained by imagining the perfect throw over and over again. He won silver that year.'

Now with ANY BRAINS AT ALL IN STROKE, we would have had that created into a protocol for survivors. But we don't have two functioning neurons anywhere in stroke leadership. 

You are completely on your own to figure out your recovery. Your medical staff has abdicated responsibility for anything to do with your recovery. Have they ever given you anything exact on what to do to recover?  Obviously not. 

Reliability and validity of the Modified Heckmatt scale in evaluating muscle changes with ultrasound in spasticity

Followup needed to see what interventions significantly reduce or cure spasticity now that you can objectively measure spasticity.

WHOM will do the research to answer this simple question?  I want specific names, because NO ONE IN STROKE TAKES RESPONSIBILTY FOR ANYTHING.

 

Reliability and validity of the Modified Heckmatt scale in evaluating muscle changes with ultrasound in spasticity

Author links open overlay panelMarisa C.MoretaD.O.¹AlanaFleetM.D.³RajivReebyeM.D., FRCPC³GinaMcKernanPhD.²MichaelBergerM.D., PhD., FRCPC⁴JordanFaragM.D.³Michael C.MuninM.D.¹²

https://doi.org/10.1016/j.arrct.2020.100071Get rights and content

Under a Creative Commons license

open access

Highlights

•

Spasticity can alter muscle architecture as viewed with ultrasound

•

Spastic muscles can appear bright termed increased echointensity (EI)

•

Spastic muscles with increased EI may respond less favorably to botulinum toxin

•

Muscle echointensity can be quantified using a Modified Heckmatt scale

•

The Modified Heckmatt scale demonstrated good reliability and validity

ABSTRACT

Objective

To determine the reliability and validity of the Modified Heckmatt scale in assessing muscle echotexture in spasticity.

Design

Prospective, observational, two-center study. Two residents and two ultrasound experienced staff physicians each rated 100 ultrasound images that were also analyzed using quantitative gray scale.

Setting

Academic ambulatory spasticity clinic.

Participants

Fifty participants (45 with upper and/or lower extremity spasticity and 5 healthy references).

Interventions

Not applicable.

Main Outcome Measure(s)

Modified Heckmatt scale ratings and quantitative grayscale scores

Results

Inter- and intra-rater ICCs were 0.76 and 0.81, respectively (p<0.001), indicating good to excellent reliability. A significant relationship was found between Modified Heckmatt scores and quantitative grayscale scores (r = 0.829 (p<0.001)).

Conclusions

The Modified Heckmatt scale demonstrated good reliability and validity to assess pathologic muscle changes that occur in patients with spasticity.

Case Western Reserve University-led team develops new approach to treat certain neurological diseases

Now we just need to know if stroke causes myelin damage. WHOM will answer that fuckingly simple question?  Then who will be conducting the research to see if this repairs myelin stroke damage? I want specific names, because NO ONE IN STROKE TAKES RESPONSIBILTY FOR ANYTHING.

 

Case Western Reserve University-led team develops new approach to treat certain neurological diseases

A team led by Case Western Reserve University medical researchers has developed a potential treatment method for Pelizaeus-Merzbacher disease (PMD), a fatal neurological disorder that produces severe movement, motor and cognitive dysfunction in children. It results from genetic mutations that prevent the body from properly making myelin, the protective insulation around nerve cells.
Using mouse models, the researchers identified and validated a new treatment target — a toxic protein resulting from the genetic mutation. Next, they successfully used a family of drugs known as ASOs (antisense oligonucleotides) to target the ribonucleic acid (RNA) strands that created the abnormal protein to stop its production. This treatment reduced PMD's hallmark symptoms and extended lifespan, establishing the clinical potential of this approach.
By demonstrating effective delivery of the ASOs to myelin-producing cells in the nervous system, researchers raised the prospect for using this method to treat other myelin disorders that result from dysfunction within these cells, including multiple sclerosis (MS).
Their research was published online July 1 in the journal Nature.
“The pre-clinical results were profound. PMD mouse models that typically die within a few weeks of birth were able to live a full lifespan after treatment,” said Paul Tesar, principal investigator on the research, a professor in the Department of Genetics and Genome Sciences at the School of Medicine
and the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics. “Our results open
the door for the development of the first treatment for PMD as well as a new therapeutic approach for
other myelin disorders.”

Paul Tesar, principal investigator, a professor in the Department of Genetics and Genome Sciences at the School of Medicine and the Dr. Donald and Ruth Weber Goodman Professor of Innovative Therapeutics.

Study co-authors include an interdisciplinary team of researchers from the medical school, Ionis Pharmaceuticals, a Carlsbad, Calif.-based pioneer developer of RNA-targeted therapies, and Cleveland Clinic. First author Matthew Elitt worked in Tesar's lab as a Case Western Reserve medical and graduate student.
PMD attacks the young
PMD is a rare, genetic condition involving the brain and spinal cord that primarily affects boys. Symptoms can appear in early infancy and begin with jerky eye movements and abnormal head movements. Over time, children develop severe muscle weakness and stiffness, cognitive dysfunction, difficulty walking and fail to reach developmental milestones such as speaking. The disease cuts life expectancy short, and people with the most severe cases die in childhood.
The disease results from errors in a gene called proteolipid protein 1 (PLP1). Normally, this gene produces proteolipid protein (PLP) a major component of myelin, which wraps and insulates nerve fibers to allow proper transmission of electrical signals in the nervous system. But a faulty PLP1 gene produces toxic proteins that kill myelin producing cells and prevent myelin from developing and functioning properly — resulting in the severe neurological dysfunction in PMD patients.
PMD impacts a few thousand people around the world. So far, no therapy has lessened symptoms or extended lifespans.
For nearly a decade, Tesar and his team have worked to better understand and develop new therapies for myelin disorders. They have had a series of successes, and their myelin-regenerating drugs for MS are now in commercial development.
Latest research
In the current laboratory work, the researchers found that suppressing mutant PLP1 and its toxic protein restored myelin-producing cells, produced functioning myelin, reduced disease symptoms and extended lifespans.
After validating that PLP1 was their therapeutic target, the researchers pursued pre-clinical treatment options. They knew mutations in the PLP1 gene produced faulty RNA strands that, in turn, created the toxic PLP protein.
So they teamed with Ionis Pharmaceuticals, a leader in RNA-targeted therapeutics and pioneer of ASOs. These short strings of chemically modified DNA can be designed to bind to a specific RNA target and block production of its protein product.
And that’s exactly what happened in their studies. The result was improved myelin and locomotion, and substantial extension of lifespan.  "ASOs provided an opportunity to cut the disease-causing protein off at its source," Elitt said.
The successful clinical use of ASOs is relatively new, yet recent developments seem promising. In 2016, the U.S. Food and Drug Administration approved the first ASO drug for a neurological disorder, spinal muscular atrophy. The drug, Spinraza, was developed by Ionis and commercialized by Biogen. More ASO therapies are in development, and clinical trials and hold promise for addressing many neurological diseases that as of now have no effective treatment options.
Tesar said that ongoing and planned experiments in his laboratory will help guide future clinical development of ASO therapy for PMD. For example, researchers want to understand more about how well the treatment works after the onset of symptoms, how long it lasts, how often treatment needs to be given and whether it might be effective for all PMD patients, regardless of their specific form of the disease.
“While important research questions remain, I’m cautiously optimistic about the prospect for this method to move into clinical development and trials for PMD patients,” Tesar said. “I truly hope our work can make a difference for PMD patients and families.”
For more information, visit .

Perfect world of stroke rehab - recovery plan

From a conversation with another survivor points out the current situation.
Not good.

Lead, Follow, or GET OUT OF THE WAY!

Doesn't this just about sum up our feelings about the role doctors and therapists should play?

The one thing that pisses me off more than any other is this.  The identification and implementation of a recovery plan is apparently NOT the responsibility of doctors or therapists.  Isn't it ironic that they still maintain that proprietary attitude when a patient appears to be trespassing into what they perceive as their realm.  They manage to dismiss our ideas while effectively providing none of their own.

I once brought in an article on hand recovery using the Saeboflex. My doctor totally dismissed it, I don't think he had even thought or researched it at all. He was just never going to listen to a patient's ideas. I was so fucking mad I left him and went to a different doctor telling him the only reason I was using him was to get the Saeboflex even though my extension was not enough to meet the criteria for use. I really hated the Saeboflex, the bead chains for adjusting the tension are almost impossible to adjust one-handed and just getting it on was an extreme challenge. When I complained to Saeboflex their excuse was that the unit was supposed to be used with a therapists help. In my opinion, bad design since all stroke rehab implements should be able to be put on solo one handed with no outside interventions. 

Perfect World!!!

With decent scientific therapy protocols this could be resolved.  
This is the 100% recovery plan.

Compound in fruit peels halts damage and spurs neuronal repair in multiple sclerosis

Now we just need to know if stroke causes myelin damage. WHOM will answer that fuckingly simple question?  Then who will be conducting the research to see if this repairs myelin stroke damage. I want specific names, because NO ONE IN STROKE TAKES RESPONSIBILTY FOR ANYTHING. Nothing ever gets solved, you, your children and grandchildren are screwed.  You can't do this without your doctor's prescription, notice the caveat about toxic at high doses.

Compound in fruit peels halts damage and spurs neuronal repair in multiple sclerosis

Newswise | April 07, 2020

Multiple sclerosis (MS), characterized by increasing muscle weakness and paralysis, has a number of treatments that help stall progression of the disease when used early on in the disease. But the current treatments can hardly reverse damage that has already occurred in brain cells called neurons. New research suggests that a compound found in the peels of fruits such as apples and prunes, and some herbs, can reduce further damage to neurons, and also help rebuild the protective sheaths covering neurons, reversing the damage.

“Although the evidence is preliminary—our data is from animal models of disease—it’s encouraging to see a compound that both halts and repairs damage in MS, in the lab,” says Guang-Xian Zhang, PhD, co-senior author and Professor of Neuroscience at the Sidney Kimmel Medical College at Thomas Jefferson University. The study was published in the Proceedings of the National Academy of Sciences (PNAS) on Monday April 6.
“There is additional work we must do to test the safety of this compound, ursolic acid” says co-senior author A.M. Rostami, MD, PhD, chair of the department of Neurology at the Vickie and Jack Farber Institute for Neuroscience – Jefferson Health. “But this is a great new lead for disease treatment.”
The researchers used a lab-grade purified form of ursolic acid in mice that had established MS disease. “Many experiments have looked at mice in the acute phase, when disease is just starting or at the peak,” says Dr. Zhang. “Instead, we tested whether this compound was effective in chronic disease, once there has already been chronic damage to tissues of central nervous system.”
Drs. Zhang, Rostami, together with first author Yuan Zhang and colleagues used an established mouse model of multiple sclerosis that develops the disease slowly over the course of its life, mimicking human disease. At about day 12, the mouse begins the acute phase of the disease, when signs of MS, partial paralysis, appear, and when currently-available medications are most effective. The researchers, however, started treating mice at day 60—a far more advanced stage of the disease when chronic tissue damage has been formed in brain and spinal cords, which needs to be repaired and regenerated.
Researchers treated the mice for 60 days, and began to see an improvement at day 20 of treatment. The mice which were paralyzed at the start of the experiment, regained the ability to walk around again, although with weakness, after treatment.
“It’s not a cure, but if we see a similar response in people, it would represent a significant change in quality of life. And most significantly, it’s a reversal, which we really haven’t seen before with other agents at such a late stage of disease,” says Dr. Zhang.
The researchers also investigated just how ursolic acid acted on cells. They observed that it suppressed Th17 cells—a type of immune cell that is one of the main drivers of the pathological autoimmune response in MS. Many currently active therapies appear to suppress Th17. But the Jefferson researchers showed that the compound could activate precursor cells to mature into much needed myelin-sheath-making cells, called oligodendrocytes.
“This maturation effect is the most crucial,” says Dr. Zhang. “Myelin-sheath-making oligodendrocytes are depleted in MS. And the stem cells that produce new oligodentrocytes are dormant and unable to mature. This compound helps activate those stem cells into making new oligodendrocytes, and is likely responsible for the reversal of symptoms we saw.”
The next steps for the investigators include testing the compound for safety. Although ursolic acid is available as a dietary supplement, it could be toxic at high doses. “There are still a number of tests to complete before the first clinical trials,” says Dr. Rostami. “However, we are moving quickly with this promising approach.”

To read more, click here.

Perception of Dementia Risk and Preventive Actions Among US Adults Aged 50 to 64 Years

Great, blame the patient. Why don't YOU TAKE RESPONSIBILITY and write up the protocols needed to prevent dementia. THAT IS WHAT LEADERS DO. 

I'm doing this.

Dementia prevention 19 ways

Don't follow me, I'm not medically trained.

 

Perception of Dementia Risk and Preventive Actions Among US Adults Aged 50 to 64 Years

Donovan T. Maust, MD, MS^1,2,3; Erica Solway, PhD, MSW, MPH²; Kenneth M. Langa, MD, PhD^2,3,4,5; et al Jeffrey T. Kullgren, MD, MS, MPH^2,3,4; Matthias Kirch, MS²; Dianne C. Singer, MPH⁶; Preeti Malani, MD, MSJ^2,4

Author Affiliations

JAMA Neurol. 2020;77(2):259-262. doi:10.1001/jamaneurol.2019.3946

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Full Text

Disease-preventing or disease-modifying treatments do not exist for Alzheimer disease or other dementias(So fucking what? Create them.). Adults may be unaware of strategies to reduce their risk¹ and resort to marketed but ineffective options, such as ginkgo biloba or vitamin E. While these so-called treatments are relatively inexpensive, new preventive therapies may not be. Thus, individuals overestimating their risk of developing dementia could lead to inappropriate use and excessive costs.² This analysis explores how adults aged 50 to 64 years estimate their lifetime risk of dementia and the risk-reducing strategies they pursue.

Full Text

Inconsistent classification of mild stroke and implications of health services delivery

 I have seen nothing that even remotely suggests that any stroke damage diagnosis is objective.  With nothing objective it is impossible to determine exactly what protocols worked and which ones to prescribe.  The prescription of E.T.(Evaluate and Treat) by the doctor to all therapists is completely showing that the doctor is taking no responsibility for survivor recovery.

Inconsistent classification of mild stroke and implications of health services delivery

Archives of Physical Medicine and Rehabilitation — Roberts PS, et al. | January 30, 2020

Researchers sought to perform a scoping review of mild stroke definitions based on stroke severity evaluations and/or clinical signs and symptoms reported in the literature. They searched PubMed, PsycINFO (Ovid), and CINAHL (EBSCO) databases added keyword combinations of a mild stroke, minor stroke, mini-stroke, mild cerebrovascular, minor cerebrovascular, transient ischemic attack, or TIA. For the final review, 62 studies were selected. Between January 2003 and February 2018, inclusion criteria were limited to articles published. It was noted that inequalities in the classification of mild stroke are evident with varying use of stroke severity assessments, measurement cut-off scores, imaging tools, and clinical or functional outcomes. Moreover, continued work is needed to establish a consensus definition of mild stroke, which directly influences treatment receipt, referral for services, and health service delivery.

Read the full article on Archives of Physical Medicine and Rehabilitation

Unilateral Spatial Neglect After Stroke: Current Insights

Your doctor will need to get the names of the persons following this up and creating a rehab protocol. We need names so we can assign responsibility. Without responsibility NOTHING WILL GET DONE. 

Unilateral Spatial Neglect After Stroke: Current Insights

Authors Gammeri R, Iacono C, Ricci R, Salatino A
Received 10 August 2019
Accepted for publication 24 December 2019
Published 10 January 2020 Volume 2020:16 Pages 131—152
DOI https://doi.org/10.2147/NDT.S171461
Checked for plagiarism Yes
Review by Single-blind
Peer reviewer comments 2
Editor who approved publication: Dr Roger Pinder

Roberto Gammeri, ¹ Claudio Iacono, ¹ Raffaella Ricci, ^{1, 2} Adriana Salatino <sup>1

1</sup>Department of Psychology, SAMBA (SpAtial, Motor and Bodily Awareness) Research Group, University of Turin, Turin, Italy; ²Neuroscience Institute of Turin (NIT), University of Turin, Turin, Italy

Correspondence: Raffaella Ricci; Adriana Salatino
Department of Psychology, Via Verdi, 10, Turin 10124, Italy
Tel +39 0116702057
Email raffaella.ricci@unito.it; adriana.salatino@unito.it

Introduction: Unilateral spatial neglect (USN) is a disorder of contralesional space awareness which often follows unilateral brain lesion. Since USN impairs awareness of contralesional space/body and often of concomitant motor disorders, its presence represents a negative prognostic factor of functional recovery. Thus, the disorder needs to be carefully diagnosed and treated. Here, we attempted to present a clear and concise picture of current insights in the comprehension and rehabilitation of USN.
Methods: We first provided an updated overview of USN clinical and neuroanatomical features and then highlighted recent progresses in the diagnosis and rehabilitation of the disease. In relation to USN rehabilitation, we conducted a MEDLINE literature research on three of the most promising interventions for USN rehabilitation: prismatic adaptation (PA), non-invasive brain stimulation (NIBS), and virtual reality (VR). The identified studies were classified according to the strength of their methods.
Results: The last years have witnessed a relative decrement of interest in the study of neuropsychological disorders of spatial awareness in USN, but a relative increase in the study of potential interventions for its rehabilitation. Although optimal protocols still need to be defined, high-quality studies have demonstrated the efficacy of PA, TMS and tDCS interventions for the treatment of USN. In addition, preliminary investigations are suggesting the potentials of GVS and VR approaches for USN rehabilitation.
Conclusion: Advancing neuropsychological and neuroscience tools to investigate USN pathophysiology is a necessary step to identify effective rehabilitation treatments and to foster our understanding of neurofunctional bases of spatial cognition in the healthy brain.

Keywords: unilateral spatial neglect, rehabilitation, spatial attention, stroke

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Does statin increase the risk of intracerebral hemorrhage in stroke survivors? A meta-analysis and trial sequential analysis

Your responsible doctor will have to do the analysis  on benefits of statins vs. risks since our fucking failures of stroke associations won't do a damn thing and write up a protocol on use.  

Statins.
tested in rats from 2003
http://oc1dean.blogspot.com/2011/09/statins-induce-angiogenesis.html 
http://oc1dean.blogspot.com/2013/02/simvastatin-attenuates-stroke-induced.html
Or,
Simvastatin attenuates axonal injury after experimental traumatic brain injury and promotes neurite outgrowth of primary cortical neurons
tested in humans, March, 2011
http://www.medwirenews.com/39/91658/Stroke/Acute_statin_therapy_improves_survival_after_ischemic_stroke.html

 

Does statin increase the risk of intracerebral hemorrhage in stroke survivors? A meta-analysis and trial sequential analysis 

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Ru Jian Jonathan Teoh, Chi-Jung Huang, Chi Peng Chan, ...

First Published July 24, 2019 Research Article

https://doi.org/10.1177/1756286419864830

Article information

Abstract

Background:

It remains debatable whether statin increases the risk of intracerebral hemorrhage (ICH) in poststroke patients.

Methods:

We systematically searched PubMed, EMBASE, and CENTRAL for randomized controlled trials. Trial sequential analysis (TSA) was conducted to assess the reliability and conclusiveness of the available evidence in the meta-analysis. To evaluate the overall effectiveness, the net composite endpoints were derived by totaling ischemic stroke, hemorrhagic stroke, transient ischemic attack (TIA), myocardial infarction, and cardiovascular mortality.

Results:

A total of 17 trials with 11,576 subjects with previous ischemic stroke, TIA, or ICH were included, in which statin therapy increased the risk of hemorrhagic stroke (risk ratio [RR], 1.42; 95% confidence interval [CI], 1.07–1.87), but reduced the risk of ischemic stroke (RR, 0.85; 95% CI, 0.75–0.95). For the net composite endpoints, statin therapy was associated with a 17% risk reduction (95% CI, 12–21%; number needed to treat = 6). With a control event rate 2% and RR increase 40%, the TSA suggested a conclusive signal of an increased risk of hemorrhagic stroke in stroke survivors taking statin. However, with the sensitivity analysis by changing assumptions, the conclusions about hemorrhagic stroke risk were less robust.

Conclusions:

Statin therapy in poststroke patients increased the risk of hemorrhagic stroke but effectively reduced ischemic stroke risk. Weighing the benefits and potential harms, statin has an overall beneficial effect in patients with previous stroke or TIA. However, more studies are required(Wow, way to take no responsibility of your work.) to investigate the conclusiveness of the increased hemorrhagic stroke risk revealed in our study.

Keywords cardiovascular events, cerebrovascular disease, meta-analysis, secondary stroke prevention, statin, trial sequential analysis

Introduction

Statins can reduce cardiovascular events and mortality among patients with coronary heart disease.^1,2 However, in patients with acute or previous history of ischemic stroke and intracerebral hemorrhage (ICH), findings on the use of statins are inconsistent. In a meta-analysis with more than 100,000 patients, statin use in patients with acute stroke was found to be associated with good functional outcomes at 3 months but not at 1 year.³ A few other meta-analyses also found that statins have no significant benefits in patients with acute stroke in reducing recurrent ischemic stroke or ICH, cardiovascular events, and mortality.^4,5 Some studies found an inverse relationship between low-density lipoprotein cholesterol (LDL-C) and the risk of ICH, and some found a risk of hemorrhagic transformation in patients using statins.^6–11 However, the Stroke Prevention by Aggressive Reduction in Cholesterol Levels (SPARCL) study found a significant risk of ICH associated with statin use in poststroke patients.⁶ A meta-analysis of four studies in 2008 investigating statin therapy in patients with cerebrovascular diseases suggested that statins reduced risk of overall and ischemic stroke but increased risk of hemorrhagic stroke.¹² However, results of many new studies for stroke survivors were reported after 2008, which provided more information about the effects of statins in poststroke patients.^13–16
Systematic review and meta-analyses of existing randomized controlled trials (RCTs) can help to summarize the totality of current existing evidence and clarify the conflicting information on the benefits and risks of statin therapy in poststroke patients. However, meta-analysis may result in random errors due to sparse data and repeated significance testing when updating a meta-analysis with new trials. Therefore, trial sequential analysis (TSA) has been developed to reduce the spurious inference from meta-analysis.¹⁷ Consequently, we performed an updated systematic review with meta-analysis and TSA of published RCTs to investigate the effect of statin therapy on stroke recurrence (including ischemic stroke and ICH), major adverse cardiovascular events (MACEs), and cardiovascular mortality, and also to evaluate its overall effectiveness in patients with previous ischemic stroke or ICH.

Methods

The prespecified protocol for this review was registered with the International Prospective Register of Systematic Reviews (PROSPERO), number CRD 42017079212, and the study report adhered to the Preferred Reporting Items for Systematic Reviews and Meta-analyses (PRISMA) guideline (Table S1).¹⁸ All analyses were based on previously published studies, thus no ethical approval and patient consent was required.

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