Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 33,919 posts. Searching is done in the search box in upper left corner. I blog on anything to do with stroke. DO NOT DO ANYTHING SUGGESTED HERE AS I AM NOT MEDICALLY TRAINED, YOUR DOCTOR IS, LISTEN TO THEM. BUT I BET THEY DON'T KNOW HOW TO GET YOU 100% RECOVERED. I DON'T EITHER BUT HAVE PLENTY OF QUESTIONS FOR YOUR DOCTOR TO ANSWER.
Changing stroke rehab and research worldwide now.Time is Brain!trillions and trillions of neuronsthatDIEeach day because there areNOeffective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.
What this blog is for:
My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.
PrecivityAD2 is the first blood-based biomarker for people as young as 40 with cognitive symptoms
The FDA cleared the PrecivityAD2 blood test to help diagnose Alzheimer's disease as part of a standard clinical workup, C2N Diagnostics announced Thursday.
The test, which measures plasma amyloid beta and tau peptide ratios to assess the likelihood of brain amyloid plaques, is the first Alzheimer's blood-based biomarker for people as young as 40 with cognitive symptoms.
PrecivityAD2 is indicated for adults with signs or symptoms of cognitive impairment being evaluated for Alzheimer's or other forms of cognitive decline. It's intended to be used with a clinical assessment to help healthcare professionals identify patients with amyloid pathology, not as a screening or standalone diagnostic test.
The test uses high-resolution mass spectrometry to quantify Alzheimer's disease biomarkers in blood, producing an outcome called the amyloid probability score 2 (APS2). The APS2 incorporates the ratio of plasma phosphorylated tau 217 (p-tau217) relative to non-p-tau217, combined with a plasma amyloid-beta 42/40 ratio, to rule in or rule out Alzheimer's disease.
In a validation study of 1,142 people with signs or symptoms of cognitive decline, PrecivityAD2 showed a 97.6% positive predictive value (rule-in) and a 93.1% negative predictive value (rule-out) to detect brain amyloid plaques using dual cutoffs measured against amyloid PET or cerebrospinal fluid testing, C2N reported. The test was effective at detecting plaques in a wide range of patients, including people with mild symptoms and those with more advanced cognitive impairment.
PrecivityAD2 showed consistent diagnostic performance as age increased and in people with comorbidities like atrial fibrillation, autoimmune or inflammatory disease, chronic heart failure or kidney disease, coronary heart disease, depression, diabetes, dyslipidemia, history of cancer, history of stroke or transient ischemic attack, hypertension, or obesity, the company added.
A recent study in Sweden showed the test was useful to help primary care physicians rule out Alzheimer's disease. Earlier research showed the APS2 score performed better than primary care doctors or dementia specialists in detecting Alzheimer's disease among people with cognitive symptoms.
In 2025, the FDA cleared two other diagnostic blood tests for Alzheimer's disease: one to help clinicians identify Alzheimer's in people with signs and symptoms, the other to rule out Alzheimer's disease in primary care.
Lab-developed tests not approved by the FDA are also on the market. Last year, the Alzheimer's Association issued guidance outlining sensitivity and specificity parameters for Alzheimer's blood tests to either triage or diagnose people with cognitive impairment.
An estimated 19 to 20 million U.S. adults 65 and older, and hundreds of thousands more between the ages of 45 and 65, have cognitive impairment and may benefit from an early diagnosis, C2N Diagnostics noted.
PrecivityAD2 can be ordered by healthcare professionals experienced in evaluating patients with cognitive impairment, the company stated. It currently is available as a lab-developed test; the FDA-cleared test version is expected to be available later this year.
Just bought a 4 level condo, 7 steps to
each level. Absolutely do not believe in removing steps in living
quarters. Don't do steps at home, won't be able to travel to step laden
places like Machu Pichu or restrooms anywhere in Europe!
Maybe you'd rather solve stroke to 100% recovery first when you are the1 in 4 per WHO that has a stroke! Just a thought. Getting 100% recovered would mean a better survival of that second stroke. Cognitive resilience and all.
James E Siegler, MD, FAHA Publish Date August 17, 2026
James Siegler, MD, FAHA, director of the Comprehensive Stroke Center at the University of Chicago, explores the evolving landscape of post-stroke care.
Ischemic stroke remains a leading cause of mortality and long-term disability worldwide, with recurrent cerebrovascular events contributing substantially to cumulative neurologic injury, functional decline, and health care burden. Although major advances in acute stroke management have significantly improved survival, secondary prevention following an index ischemic stroke continues to represent a critical challenge in contemporary cerebrovascular care.
Of the more than 800,000 strokes in the US every year, 1 in 4 are recurrent events.1 The risk for recurrent stroke varies widely across patient populations and stroke phenotypes, ranging from 10% to 15% within 12 months among patients with advanced microvascular disease or large artery atherosclerosis.2 This risk persists despite advances in risk factor modification and the widespread availability of evidence-based guidelines and online resources, highlighting gaps between recommended care and real-world implementation. Barriers including health care access, treatment adherence, economic burden, patient engagement, and uncertainty in individualized risk assessment continue to limit the effectiveness of secondary prevention strategies. Closing the gap between clinical evidence and real-world implementation remains essential to reducing recurrent stroke burden and improving functional outcomes among stroke survivors. Despite these challenges, most funding in cerebrovascular research continues to emphasize innovative technologies and pharmacotherapies, with comparatively less emphasis on translational research and implementation gaps.
Present Day Stroke Care
Persistent Risk After Index Stroke
The risk for recurrent ischemic stroke remains substantial throughout both early and late periods following the index event. After the acute period — when recurrent stroke risk is highest, typically within the first few weeks after stroke — the underlying mechanism (eg atrial fibrillation or an unstable atherosclerotic plaque) is often identified, and individualized treatment is initiated. However, long-term risk persists well beyond the immediate post-stroke period. Longitudinal cohort studies consistently demonstrate sustained elevation in recurrent stroke risk over subsequent years, driven by persistent and uncontrolled vascular risk factors, including hypertension, dyslipidemia, obesity, diabetes mellitus, atrial fibrillation, obstructive sleep apnea, substance use (including tobacco and alcohol), and systemic vascular dysfunction.3 Without effective risk factor modification, the likelihood of recurrent stroke or other vascular events remains considerable. Perhaps more importantly, recurrent cerebrovascular events often result in greater cumulative disability than the initial stroke, contributing to progressive neurologic impairment, reduced functional independence, dementia, and diminished quality of life. These events also have substantial downstream consequences, including increased caregiver burden and higher health care costs for patients and health systems. Among the many limitations in successful secondary stroke prevention strategies is fragmentation of post-discharge care delivery. Stroke survivors frequently transition from hospitalization to outpatient care characterized by delayed or unscheduled stroke specialist follow-up, inadequate coordination between inpatient and ambulatory care teams, and limited access to multidisciplinary prevention services. These structural barriers are particularly pronounced in geographically underserved and rural populations, where access to vascular neurology, cardiology, rehabilitation medicine, and comprehensive stroke centers remains limited. Follow-up care is essential for reinforcing the benefits of antithrombotic therapy, lipid-lowering treatments, dietary and lifestyle modifications, and recognition of stroke warning signs and symptoms. Because many stroke risk factors are clinically silent, particularly hypertension, dyslipidemia, and diabetes, ongoing follow-up with primary and subspecialty care providers is necessary to ensure patients achieve target blood pressure, cholesterol, and glycemic goals.
Economic and Structural Challenges in Long-Term Care
The economic burden of long-term stroke management represents another important challenge to successful secondary prevention. Effective post-stroke care often requires prolonged pharmacotherapy, outpatient specialist visits, repeat diagnostic testing, rehabilitation services, and management of multiple chronic conditions. Out-of-pocket costs, insurance limitations, prescription drug costs, transportation challenges, geographic barriers to subspecialty care, and restricted access to rehabilitation services can all impair adherence to recommended care. Although strategies such as out-of-network exemptions, teleneurology appointments, and partially subsidized pharmacy coverage may help address some barriers, they do not fully resolve challenges to effective secondary prevention. These financial and structural barriers disproportionately affect socioeconomically vulnerable populations and contribute to persistent disparities in recurrent stroke outcomes.
Future State of Stroke Care
Residual Stroke Risk Despite Optimal Care
Even if all barriers to medical care are limited for a given patient, the risk for recurrent stroke remains unacceptably high. This may reflect the chronic and progressive nature of atherosclerotic vascular disease, although the primary drivers of residual stroke risk remain incompletely understood. For example, less than 25% of carotid plaque burden is explained by traditional vascular risk factors.4 Other contributors to vascular disease, inflammation, and stroke risk may include genetic variation, pathologic metabolites originating from the gut microbiome, microplastics, and other patient-level factors.
Although advances in pharmacotherapies for secondary stroke prevention now include individualized antithrombotic regimens, more aggressive lipid targets, and glucagon-like peptide agonists, improvements in stroke prevention remain incremental.
Expanding the Secondary Prevention Toolkit
In addition to the persistent biological drivers of stroke risk, limitations of current therapies highlight the need for continued innovation. Concerns regarding medication toxicity and growing distrust of health care providers have introduced new challenges to sustained treatment.
Nearly a quarter century ago, aspirin became a mainstay of secondary prevention, with a number-needed-to-treat (NNT) of approximately 100 to prevent 1 stroke at 2 weeks.5 However, long-term use is associated with risks for gastrointestinal bleeding or renal dysfunction. A decade later, high-intensity statins expanded the pharmacologic armamentarium, with an NNT of 45 to prevent stroke after 5 years of sustained treatment.6 Yet, more than half of high-risk patients discontinue statins over time due to non-adherence, perceived side effects, or financial barriers.7
Further, glucagon-like peptide agonists have been shown to promote weight loss, reduce tobacco and alcohol use, and lower stroke rates among patients with diabetes and/or obesity, but more than one-third of patients discontinue these therapies at 1 year due to a combination of adverse effects, high out-of-pocket costs, and access barriers.8
There is no single solution or “silver bullet” for secondary stroke prevention. However, emerging therapies may offer new opportunities. Asundexian, a novel factor XIa inhibitor, has been recently shown to reduce recurrent stroke in patients with noncardioembolic stroke.9 With an NNT of 45 to prevent 1 stroke over 19 months and no significant risk for major or minor bleeding, this therapy may represent an important advance in secondary stroke prevention. The Phase III LIBREXIA-Stroke trial (ClinicalTrials.gov Identifier: NCT05702034) evaluating milvexian is ongoing and may provide additional insight into a class effect for factor XIa inhibitors.
Toward Precision Stroke Prevention
As the understanding of stroke biology expands, future approaches will likely move toward more individualized risk prediction and treatment selection. For patients with elevated lipoprotein(a), a low-density lipoprotein molecule largely determined by genetics, Phase III trials are ongoing that are evaluating whether small molecules or small interfering RNA therapies can reduce vascular events. Phase II trials of subcutaneously administered pelacarsen, olpasiran, lepodisiran, muvalaplin, and zerlasirin have demonstrated 30 to 95% reductions in lipoprotein(a) levels, with generally mild injection site pain and flu-like symptoms.10 Whether these reductions translate into meaningful clinical benefit remains uncertain.
The future of secondary stroke prevention will be increasingly personalized. Advances in prolonged cardiac rhythm monitoring, wearable diagnostic technologies, biomarker-based risk stratification, and artificial intelligence-driven predictive modeling may improve identification of patients at highest risk for recurrent cerebrovascular events. Precision medicine approaches are also being explored to guide individualized antithrombotic therapy based on stroke mechanism and patient-specific risk profiles.
In parallel, digital health platforms, remote physiologic monitoring, and telemedicine-based care models may improve longitudinal patient engagement, medication adherence, and access to specialist care, particularly among underserved populations.
Closing the Evidence-to-Practice Gap
Reducing recurrent ischemic stroke risk and minimizing long-term disability will require more than the continued application of established evidence-based therapies. Persistent implementation barriers, including fragmented care delivery, suboptimal adherence, financial burden, patient mistrust, and uncertainty in individualized therapeutic decisions, continue to limit the effectiveness of current prevention strategies.
Future progress in secondary stroke prevention will depend not only on therapeutic innovation but also on scalable, cost-effective health care delivery models capable of translating scientific advances into durable improvements in cerebrovascular outcomes. Closing the gap between clinical evidence and real-world implementation remains essential to reducing recurrent stroke burden and improving functional outcomes among stroke survivors.
The mitochondria is the “powerhouse of the cell,” but B12 is what keeps the lights on. Here’s the latest science on how it affects your energy levels.
Protein powder, creatine, pre-workouts … There are more supplements than ever promising to elevate your performance in the gym. But if you walked into a supplement shop asking for vitamin B12 for muscle growth, you’d probably raise a few eyebrows.
B12 isn’t typically the go-to nutrient for muscle mass. But recent scientific evidence indicates the “energy vitamin,” may also play a role in powering your muscles. Here’s what we know, and how you can capitalize on it.
What You Should Know About B12 and Your Muscles
When we think of eating to fuel our muscles, you’ve probably heard about eating more protein and consuming enough calories. Physically active folks use their muscles more, so they need larger quantities of these major fuel sources.
But protein alone can’t do it all, and the research shows that other nutrients, like vitamin B12, may matter too. Vitamin B12 is essential for DNA synthesis, healthy nerve function, and red blood cell production — all of which help support normal muscle function.
Particularly, vitamin B12 supports the mitochondria, also known as those famous cellular “power plants” that provide energy.
It’s possible that insufficient vitamin B12 intake can depower your muscles’ capabilities. In fact, researchers believeage-related losses in muscle may have to do with mitochondrial dysfunction.
Are You at Risk of B12 Deficiency?
While the majority of B12 sources in our diet come from animal foods, only about half is effectively absorbed.
What’s more, deficiency is more common in some groups than others. Particularly, adults over 50, vegans and vegetarians, people with digestive conditions, and anyone who’s had stomach surgery may all be at an increased risk for low B12 levels. Plus, some medications may interfere with absorption as well.
There may be a connection between low vitamin B12 status and feeling strong, according to Caroline Thomason Bunn, RD. “Supplementing with vitamin B12 has been shown to improve strength and physical function in elderly adults who were deficient,” she shares.
Vitamin B12 deficiency goes beyond making you feel tired. It’s linked to anemia, nerve symptoms, muscle weakness, and even cognitive impairment in older people. It saps your muscles of an essential mechanistic puzzle piece, according to the latest research.
Going Deeper on the B12–Mitochondria Link
In 2026, scientists from Cornell University and the University of Alabama at Birmingham set out to determine how vitamin B12 deficiency affects skeletal muscle. Rodent subjects were split into two groups:
Young-adult male mice that were either genetically unable to use B12 properly or fed a B12-deficient diet for seven weeks.
Older mice (comparable to senior humans in age) that received weekly B12 injections for eight weeks.
Credit: iStock/Professor25
In the B12-deficient group, the researchers observed that the mitochondria were not functioning at optimal capacity — the mice muscles in this group generated and burned about 25 percent less energy.
But the more useful question is whether that translates to actual strength — and human research suggests it can. In a 2024 pilot study, older adults with mild B12 deficiency who supplemented for three months saw significant gains in muscle strength and quality, reaching about the same level as people whose B12 was already healthy.
Before we get practical, bear in mind the mouse study points to a mechanism rather than proof — and the human evidence, while encouraging, is still one small pilot in people who were already deficient.
The Takeaway
Vitamin B12 supplementation has been recommended by institutions like the Mayo Clinic for years, but when it comes to muscle health and functionality, other supplements tend to steal the spotlight.
Especially if you’re over 50. Incorporate vitamin B12-rich foods into your diet to ensure you meet the recommended daily intake. Some good sources of B12 to include in your diet are:
Clams
Beef liver
Tuna
Salmon
Eggs
Fortified nutritional yeast
Fortified breakfast cereals and other grains
And since B12 supports the mitochondria in your muscles, pairing it with enough protein and regular strength training may help you hold onto muscle function as you age.
Bottom Line
Here’s what we know: Getting adequate micronutrients, such as vitamins like B12, is just as important as hitting the big benchmarks — even if you don’t always feel the effects right away.
Feeling strong and energetic can make a massive difference in your overall quality of life, but requires you to pay attention to more than just calories or protein. If you’re feeling fatigued and are part of a cohort that tends to suffer from B12 deficiency, upping your intake might make a noticeable difference.
That said, the clearest human evidence so far is a small pilot where three months of B12 brought deficient older adults’ strength up to match non-deficient peers — promising, but larger trials are the next step, especially on whether B12 supplementation helps people who aren’t prone to deficiencies. In the meantime, there’s no harm in keeping your bases covered.
Experts Who Contributed
Jake Dickson (BS-EXS, NASM-CPT), wrote this article.
Lauren Keary, NASM-CNC, reviewed this article for accuracy.
Caroline Thomason Bunn, RD, CDCES, founder of Caroline Thomason Nutrition, reviewed this article for accuracy.
supports the mitochondria, also known as those famous cellular “power plants” that provide energy.
It’s possible that insufficient vitamin B12 intake can depower your muscles’ capabilities. In fact, researchers believeage-related losses in muscle may have to do with mitochondrial dysfunction.
Are You at Risk of B12 Deficiency?
While the majority of B12 sources in our diet come from animal foods, only about half is effectively absorbed.
What’s more, deficiency is more common in some groups than others. Particularly, adults over 50, vegans and vegetarians, people with digestive conditions, and anyone who’s had stomach surgery may all be at an increased risk for low B12 levels. Plus, some medications may interfere with absorption as well.
There may be a connection between low vitamin B12 status and feeling strong, according to Caroline Thomason Bunn, RD. “Supplementing with vitamin B12 has been shown to improve strength and physical function in elderly adults who were deficient,” she shares.
Vitamin B12 deficiency goes beyond making you feel tired. It’s linked to anemia, nerve symptoms, muscle weakness, and even cognitive impairment in older people. It saps your muscles of an essential mechanistic puzzle piece, according to the latest research.
Going Deeper on the B12–Mitochondria Link
In 2026, scientists from Cornell University and the University of Alabama at Birmingham set out to determine how vitamin B12 deficiency affects skeletal muscle. Rodent subjects were split into two groups:
Young-adult male mice that were either genetically unable to use B12 properly or fed a B12-deficient diet for seven weeks.
Older mice (comparable to senior humans in age) that received weekly B12 injections for eight weeks.
Credit: iStock/Professor25
In the B12-deficient group, the researchers observed that the mitochondria were not functioning at optimal capacity — the mice muscles in this group generated and burned about 25 percent less energy.
But the more useful question is whether that translates to actual strength — and human research suggests it can. In a 2024 pilot study, older adults with mild B12 deficiency who supplemented for three months saw significant gains in muscle strength and quality, reaching about the same level as people whose B12 was already healthy.
Before we get practical, bear in mind the mouse study points to a mechanism rather than proof — and the human evidence, while encouraging, is still one small pilot in people who were already deficient.
The Takeaway
Vitamin B12 supplementation has been recommended by institutions like the Mayo Clinic for years, but when it comes to muscle health and functionality, other supplements tend to steal the spotlight.
Especially if you’re over 50. Incorporate vitamin B12-rich foods into your diet to ensure you meet the recommended daily intake. Some good sources of B12 to include in your diet are:
Clams
Beef liver
Tuna
Salmon
Eggs
Fortified nutritional yeast
Fortified breakfast cereals and other grains
And since B12 supports the mitochondria in your muscles, pairing it with enough protein and regular strength training may help you hold onto muscle function as you age.
Bottom Line
Here’s what we know: Getting adequate micronutrients, such as vitamins like B12, is just as important as hitting the big benchmarks — even if you don’t always feel the effects right away.
Feeling strong and energetic can make a massive difference in your overall quality of life, but requires you to pay attention to more than just calories or protein. If you’re feeling fatigued and are part of a cohort that tends to suffer from B12 deficiency, upping your intake might make a noticeable difference.
That said, the clearest human evidence so far is a small pilot where three months of B12 brought deficient older adults’ strength up to match non-deficient peers — promising, but larger trials are the next step, especially on whether B12 supplementation helps people who aren’t prone to deficiencies. In the meantime, there’s no harm in keeping your bases covered.
Experts Who Contributed
Jake Dickson (BS-EXS, NASM-CPT), wrote this article.
Lauren Keary, NASM-CNC, reviewed this article for accuracy.
Caroline Thomason Bunn, RD, CDCES, founder of Caroline Thomason Nutrition, reviewed this article for accuracy.
