Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective 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.

Wednesday, July 22, 2026

Dementia Prevention Is Not One-Size-Fits-All, Study Shows

 Does your competent? doctor have ANY SIZES AT ALL FOR EXACT DEMENTIA PREVENTION? Is s/he at least working with researchers to get protocols written? If not, fire that doctor!

Dementia Prevention Is Not One-Size-Fits-All, Study Shows

Modifiable dementia risk factors varied widely from country to country and a one-size-fits-all approach to dementia prevention will not work everywhere, data from 14 countries and regions showed.

Both differences and similarities emerged in a global analysis of risks for 214,000 older adults, reported Emma Nichols, PhD, of the University of Southern California in Los Angeles, at the Alzheimer's Association International Conference.

Low education was a prevalent dementia risk factor for 85.6% of people in China compared with 12.0% of Americans, Nichols said. Obesity was a risk factor for 44.9% of older adults in the U.S., but only 13.3% of people in India.

Despite differences in prevalence, similar factors -- like cardiovascular risks (high cholesterol, hypertension, and diabetes) or risky behaviors (smoking and drinking) -- tended to cluster together. Poor hearing, poor vision, and low education also co-occurred frequently.

Risk factors often overlapped, with more than 50% of individuals having at least two risk factors, Nichols pointed out. In 11 countries and regions, the prevalence of at least four risk factors exceeded 20%.

The findings were published in Lancet Healthy Longevity.

"To create policies and programs that can help lower the burden of dementia, we need to understand where dementia risk factors are most common and how they differ across countries," Nichols said.

"This study offers the most detailed international data to date on how dementia risk factors vary from place to place. The findings show both important differences and shared patterns across settings," she told MedPage Today.

"This information can help governments, health systems, and communities design better prevention efforts focusing not only on individual risk factors, but also on the broader social and structural conditions that impact dementia risk," Nichols added.

The findings have direct implications for dementia prevention, noted Michal Schnaider Beeri, PhD, of Rutgers University in New Brunswick, New Jersey, and Yian Gu, MD, MS, PhD, of Columbia University in New York City.

"The consistent emergence of cardiovascular, behavioral (smoking and excessive alcohol consumption), and sensory-social clusters provides empirical support for multidomain intervention models and suggests that prevention strategies tailored to these clusters might be both efficient and necessary," Beeri and Gu wrote in a comment accompanying the study.

It's not clear whether interventions structured around these empirically derived clusters would outperform the existing multidomain approaches used in the POINTER and FINGER trials, they observed.

"The cross-sectional design of the study also precludes assessment of how risk profiles evolve over time," they added.

In 2024, the Lancet Commission identified 14 risk factors that were linked with dementia. Most evidence in the commission's report came from high-income countries, creating a knowledge gap about risks in other places.

Using the Gateway to Global Aging platform, Nichols and colleagues combined harmonized survey data collected between 2009 and 2023 from 214,251 participants in 11 long-running studies of aging in 14 places -- the U.S., England, Ireland, Northern Ireland, four regions of Europe, Korea, Mexico, China, Malaysia, Brazil, and India. U.S. data came from the Health and Retirement Study.

The researchers analyzed 12 of the Lancet Commission's risk factors that were commonly available in the studies: low education, hearing loss, high LDL cholesterol, depression, physical inactivity, diabetes, smoking, hypertension, obesity, excessive alcohol use, social isolation, and vision loss. They evaluated the prevalence of each risk factor and patterns of occurrence.

Low education (particularly in low-income and middle-income countries), hypertension, and smoking were among the most prevalent risk factors in most areas. In the U.S., hypertension, smoking (former or current), high LDL cholesterol, obesity, and physical inactivity were the five most prevalent dementia risk factors.

The analysis was restricted to the risk factors reported in the Lancet Commission report and future updates should include additional variables as new evidence emerges, Nichols noted.

The researchers used binary versions of all risk factors to simplify interpretation comparisons. In some cases, continuous measures -- pack-years of smoking, for example -- can provide more detailed information.

Disclosures

Faster Cognitive Decline Linked to Cumulative Physiologic Stress

 

With your massive stress from your incompetent doctor not having 100% recovery protocols maybe you want a better doctor. Or the proper solution; EXACT 100% RECOVERY PROTOCOLS! Will your replacement doctor at least get 100% recovery protocols going?

Faster Cognitive Decline Linked to Cumulative Physiologic Stress

Higher cumulative physiologic stress reflected in salivary  was associated with faster cognitive decline, a prospective study showed.

Older adults with high cumulative cortisol exposure had worse composite global cognition scores over time, reported Ted K. S. Ng, PhD, of Rush University Medical Center in Chicago, at the Alzheimer's Association International Conference. The findings were published in JAMA Network Open.

A moderate level of intra-day cortisol variability was associated with slower cognitive decline, Ng said. Black and white participants had different cortisol profiles at baseline, but associations between cortisol and cognitive decline were similar across racial groups.

"Our study suggests that how cortisol fluctuates across the day may provide important insights into cognitive aging," Ng noted.

"We examined five complementary indices capturing three key physiological dimensions of diurnal cortisol regulation -- intra-day variability, cumulative daily exposure, and diurnal change -- rather than relying on a single cortisol measure," he told MedPage Today. "We found that these different dimensions showed distinct relationships with cognitive aging, suggesting that different aspects of stress physiology may provide complementary insights."

Cortisol follows a circadian rhythm with a sharp post-awakening rise and a gradual decline across the day. It crosses the blood-brain barrier and binds receptors in regions critical for cognition.

Changes in hypothalamic-pituitary-adrenal (HPA) axis activity have been implicated in cognitive aging, Ng and colleagues noted. It's not clear how prospective associations between cortisol and cognitive outcomes may differ by race, they added.

The researchers followed 3,895 people in the Chicago Health and Aging Project for up to 11 years. The cohort included 2,503 Black and 1,392 white participants; the mean age was 77.

Participants provided three salivary cortisol samples across a single day (waking, afternoon, and bedtime) and had repeated cognitive assessments.

"A major strength of the study is its scale and diversity," Ng pointed out. "We studied nearly 4,000 community-dwelling older adults, including more than 60% women and more than 60% Black participants, making this one of the largest and most racially diverse population-based studies of salivary cortisol and cognitive aging."

All baseline cortisol indices were associated with cross-sectional cognitive performance. "Although Black participants had distinct baseline diurnal cortisol profiles, including a more blunted diurnal rhythm, the associations between cortisol indices and cognitive outcomes were broadly similar across Black and white participants," Ng said.

"This suggests that while patterns of diurnal cortisol may differ between populations, their relationships with cognitive aging may be broadly consistent," he added. "Further research is needed to better understand the factors underlying these baseline differences."

No significant associations between cortisol and incident Alzheimer's disease were seen over the follow-up period. "This likely reflects several factors, including the substantially smaller subset with adjudicated Alzheimer's disease, the relatively small number of incident cases, and the shorter follow-up relative to the long preclinical course of Alzheimer's disease," Ng noted.

"An alternative, and not mutually exclusive, interpretation is that alterations in diurnal cortisol patterning may be more informative as early physiological indicators of neurocognitive aging than of shorter-term clinical Alzheimer's disease incidence," he added.

The findings were based on a single day of cortisol sampling. Multi-day sampling may improve reliability of within-person variability and show longer-term HPA-axis dynamics, but a single-day protocol over multiple time points is commonly used in large epidemiologic studies, the researchers noted. The study also did not measure perceived stress.

"As stress-related health challenges have become increasingly important public health concerns, our findings reinforce the need to better understand how different aspects of stress physiology influence brain health over time," Ng said.

"Because salivary cortisol is non-invasive, relatively inexpensive, and feasible to collect repeatedly outside clinical settings, it represents a promising research tool for large-scale population studies investigating stress biology, brain health, and aging," he added.

Judy George covers neurology and neuroscience news for MedPage Today, writing about brain aging, Alzheimer’s, dementia, MS, rare diseases, epilepsy, autism, headache, stroke, Parkinson’s, ALS, concussion, CTE, sleep, pain, and more. Connect:

Tuesday, July 21, 2026

Neuroplasticity in Post-Stroke Adults: Mechanisms, Modulators, and Rehabilitation Strategies: A Literature Review

 You've proven you know nothing about why a neuron gives up its' current function and takes on a neighbor's function! Figuring that out would make neuroplasticity repeatable on demand!

Neuroplasticity in Post-Stroke Adults: Mechanisms, Modulators, and Rehabilitation Strategies: A Literature Review

 Jinal Choudhari, MD 
Namita Ruhela, Ph,D.
Marti Echols, Ph,D.

Abstract

Cerebrovascular stroke remains a leading cause of long-term disability and motor impairment worldwide. Although the adult brain possesses less regenerative capacity than the pediatric nervous system, it retains a significant ability to reorganize neural networks through neuroplasticity. Understanding the biological mechanisms that govern post-stroke neuroplasticity is essential for optimizing recovery and rehabilitation outcomes. This narrative review synthesizes current evidence on the cellular and molecular pathways underlying neuroplastic changes following stroke and examines key modulators, including epigenetic regulation, neuroinflammation, sleep, environmental enrichment, and pharmacological interventions. Relevant peer-reviewed studies, systematic reviews, and preclinical investigations were analyzed to provide a comprehensive overview of the field. Current evidence suggests that adult post-stroke neuroplasticity is a dynamic and therapeutically modifiable process. Multimodal rehabilitation programs, targeted epigenetic therapies, anti-inflammatory strategies, and emerging technologies such as stem cell therapy and optogenetics represent promising avenues for enhancing neurological recovery, particularly during the critical 3-6 month period following stroke.

More at link.

Does Levetiracetam Prevent Post-Traumatic Epilepsy After TBI?

 What is your competent? doctors EXACT PROTOCOL  to prevent post-stroke epilepsy and seizures?

Does Levetiracetam Prevent Post-Traumatic Epilepsy After TBI?

Levetiracetam did not prevent late post-traumatic epilepsy and was associated with a higher burden of adverse outcomes despite reducing early epilepsy risk in patients with severe traumatic brain injury.

Prophylactic levetiracetam is associated with reduced risk for early epilepsy after severe traumatic brain injury (TBI) but not with reduced risk for long-term epilepsy, according to study results published in the Annals of NeurologyPatients with TBI are often prescribed ASMs to prevent post-traumatic epilepsy. However, current recommendations are largely based on older phenytoin and valproate trials and do not incorporate large-scale evidence evaluating levetiracetam, the current agent of choice.

Researchers used data from the TriNetX Research Network to examine the effectiveness and safety of prophylactic levetiracetam for preventing post-traumatic epilepsy after TBI. Patients (N=51,263) were assessed on the basis of whether they received levetiracetam (n=14,630) or no ASMs (n=34,226). Mild TBI was defined as a Glasgow Coma Scale (GCS) score of 13 to 15, moderate TBI as a GCS score of 9 to 12, severe TBI as a GCS score of 3 to 8, early epilepsy as onset within 7 days of injury, and late epilepsy as onset between day 7 and 1 year after injury. Our findings challenge widespread use of levetiracetam and suggest that prophylaxis should not be offered indiscriminately.

The levetiracetam and no ASM cohorts comprised 31.0% and 35.8% women (P <.0001), had a mean (SD) age of 53.9 (20.5) and 47.9 (20.5) years (P <.0001), included 28.9% and 31.2% non-White patients (P <.0001), and included 34.7% and 17.9% of patients with severe TBI, respectively (P <.0001).

Overall, epilepsy occurred in 6.7% of participants, and 14.1% died within 1 year of injury. Epilepsy within 1 year of injury was more frequent among patients with moderate (12.1%) and severe (11.3%) TBI than among those with mild TBI (4.8%; P <.001). Similarly, mortality was higher among patients with severe (39.0%) and moderate (15.7%) TBI than among those with mild TBI (4.7%; P <.001).

After adjustment for potential confounders, levetiracetam was associated with reduced risk for early epilepsy among patients with severe TBI (hazard ratio [HR], 0.545; 95% CI, 0.306-0.969; P =.039). Independent predictors of early epilepsy in this cohort included traumatic subdural hemorrhage, left cerebral contusion or laceration, craniectomy or craniotomy, and routine electroencephalography (EEG).

The researchers observed no significant association between prophylactic levetiracetam and late epilepsy overall or among patients with mild or severe TBI (HR range, 0.897-1.001). Levetiracetam was associated with lower risk for mortality through 1 year in the overall cohort (HR, 0.826; 95% CI, 0.787-0.867; P <.001) and among individuals who survived longer than 7 days after injury (HR, 0.881; 95% CI, 0.815-0.952; P =.001). However, in a sensitivity analysis limited to patients who survived longer than 7 days after injury, levetiracetam was not associated with a reduced risk for early epilepsy, including among patients with severe TBI.

Across 5 years of follow-up, patients who received levetiracetam had higher rates of mortality (difference, 2.2%; P <.0001), impaired memory or awareness (difference, 5.4%; P <.0001), migraine and headache (difference, 4.3%; P <.0001), metabolic disorders (difference, 2.6%; P <.0001), and malaise and fatigue (difference, 2.0%; P <.0001), among other adverse outcomes.

Study limitations include the inability of the TriNetX dataset to determine the sequence of events on the day of injury, preventing investigators from establishing whether levetiracetam was administered before seizure onset.

The researchers concluded, “In this large, severity-stratified cohort study, prophylactic levetiracetam reduced the risk of early seizures only in patients with severe TBI, without preventing late posttraumatic epilepsy and while conferring a substantial burden of adverse outcomes.” They continued, “Our findings challenge widespread use of levetiracetam and suggest that prophylaxis should not be offered indiscriminately.”

How Much Water Should You Drink Daily? Science-Backed Hydration Guide by Super Age

 

Another protocol for your doctor to have in place to make sure you leave the hospital better than you came in. 

Which means you probably need to be catheterized or diapered immediately in the hospital. There aren't enough nurses to get all their patients safely to the bathroom in time. When I'm traveling, especially on airplanes and buses, I purposely stay dehydrated in order not to need to use the bathroom.

On coffee:

The caffeine in coffee gives it diuretic effects, meaning it causes your body to pass more urine. But these effects are too mild to cause dehydration, especially if you're a regular coffee drinker. Coffee may even be hydrating for some people, because it contains a lot of water.

On alcohol:

For reference, a standard drink—12 ounces of beer, 5 ounces of wine, 1.5 ounces of liquor—has 14 grams of alcohol, according to the National Institute on Alcohol Abuse and Alcoholism [3]. In other words, the alcohol alone in one standard drink can make your body produce a little less than half a cup of pee.

So to calculate; a standard 5 ounce glass of wine produces less than 4 ounces of pee. That doesn't sound like dehydration.  Beer would make even better sense.

 The latest here:

How Much Water Should You Drink Daily? Science-Backed Hydration Guide

The MIND Diet Slows the Physical Aging of the Brain Itself by Super Age

 

Ask your competent? doctor for EXACT DIET PROTOCOLS! None of this MIND diet guidelines; they have NO specifics! You need SPECIFICS!

How the hell else is your incompetent? doctor recovering your 5 lost years of brain cognition due to your stroke?

Do you prefer your doctor, hospital and board of director's incompetence NOT KNOWING? OR NOT DOING? Your choice; let them be incompetent or demand action!

The MIND Diet Slows the Physical Aging of the Brain Itself

Study Maps Accelerated Brain Aging Signatures Across 9 Conditions

 Your competent? doctor has to prevent MCI post stroke! WHAT ARE THE EXACT PROTOCOLS TO DO THAT? Sorry, there aren't any, are there?

Study Maps Accelerated Brain Aging Signatures Across 9 Conditions

Summary: Researchers evaluated structural MRI scans from 45,900 controls and 2,698 individuals across 9 conditions to map brain aging signatures. Measuring Predictive Age Difference (PAD), the team found that Alzheimer’s disease and mild cognitive impairment showed the highest accelerated brain aging, followed by psychiatric disorders and substance addiction.

ADHD and autism showed no increase in PAD. The study mapped distinct regional aging patterns, such as default mode network involvement in addiction and frontal-temporal acceleration in psychiatric conditions, offering new structural biomarkers for clinical neuroscience.

Key Facts

  • Accelerated Aging Rankings: Neurodegenerative conditions (Alzheimer’s disease and MCI) showed the highest overall positive PAD (most pronounced accelerated brain aging), followed by psychiatric disorders and substance addictions.
  • Neurodevelopmental Divergence: Attention-deficit/hyperactivity disorder (ADHD) and autism spectrum disorder (ASD) showed no significant increase in PAD compared to healthy controls, indicating that neurodivergence does not equate to accelerated structural brain aging.
  • Regional Aging Signatures:
    • Prefrontal Cortex: Exhibited elevated PAD broadly across multiple brain disorders.
    • Frontal & Temporal Lobes: Showed elevated PAD specifically associated with psychiatric disorders.
    • Frontal & Occipital Cortex: Showed localized accelerated aging signature patterns in dementia.
    • Default Mode & Salience Networks: Showed selective elevated PAD tied to alcohol and tobacco addiction, alongside structural shifts in the putamen and thalamus.
  • Transcriptomic Link: Regional PAD maps correlated with condition-specific gene transcription patterns, offering biological insights into the pathways underlying accelerated structural decline.

Source: PLOS

People with dementia, mild cognitive impairment, alcohol addiction, or psychiatric disorders such as schizophrenia show increased brain aging, each in specific patterns within the brain, according to a study published July 21st in the open access journal PLOS Medicine by Shile Qi from the Nanjing University of Aeronautics and Astronautics, China, and colleagues.

Some conditions can make the brain age faster. Scientists calculate how old the brain is relative to the body using the predictive age difference (PAD), the difference between chronological age and the age predicted by brain imagine, where a positive PAD indicates that aging is accentuated or increased.

To better understand how brain disorders and divergences might affect brain aging, the authors of this study collected structure magnetic resonance imaging (MRI) data from 45,900 controls across several brain imaging banks, and compared them with of 2,698 patients with different brain conditions and differences, including attention-deficit/hyperactivity disorder (ADHD), autism spectrum disorder (ASD), alcohol or tobacco addiction, Alzheimer’s disease (AD), mild cognitive impairment (MCI), schizophrenia, bipolar disorder or major depressive disorder.

The authors found that neurodegenerative disorders of AD and MCI had the largest association with a high PAD. Addiction and psychiatric disorders were also associated with increased PAD. In contrast, there were no differences in PAD between people with ADHD or ASD and controls.

The researchers also looked at PAD values in specific areas of the brain, and examined which genes showed increased expression in people with different brain conditions.

The prefrontal cortex showed higher PAD across brain disorders. Higher PAD in the frontal and temporal lobes was associated with psychiatric disorders, while high PAD in the frontal and occipital cortex was associated with dementia.

Addiction was connected with high PAD in the default mode network, and in the salience network and the putamen and thalamus. There were also differences in gene transcription that associated with specific conditions and divergences.

While the results are correlational, and not causal, and while some conditions such as psychiatric disorders and addiction have high co-occurrence, the author suggest that understanding more about PAD could help provide biomarkers for commonly occurring brain disorders.

The authors add, “Different neurological disorders appear to leave different signatures on the brain aging clock, which may help researchers better understand the neural and biological pathways involved in these conditions.”

Funding: This work was supported by the Key Research and Development Plan of Jiangsu Province, China (BE2023668, https://kxjst.jiangsu.gov.cn) to S.Q., and the National Natural Science Foundation of China (62376124, https://www.nsfc.gov.cn) to S.Q. The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.

Key Questions Answered:

Q: What is Predictive Age Difference (PAD) and how is it measured?

A: Predictive Age Difference (PAD) is calculated by comparing a person’s actual chronological age with their estimated “brain age,” derived from structural MRI scans analyzed via machine learning algorithms. A positive PAD value indicates that the structural features of the brain resemble those of a chronologically older individual, signaling accelerated brain aging.

Q: Do all mental health conditions accelerate brain aging?

A: No. While neurodegenerative conditions (like Alzheimer’s and MCI), psychiatric disorders (like schizophrenia and major depression), and addictions (alcohol and tobacco) showed increased PAD, neurodevelopmental conditions like ADHD and autism spectrum disorder (ASD) showed no increase in brain aging compared to healthy controls.

Q: Why are regional “signatures” of brain aging important for clinical research?

A: Broad brain aging metrics only tell part of the story. By mapping accelerated aging to specific circuits, such as the default mode network in addiction or the temporal lobe in psychiatric illness, researchers can identify distinct biological pathways, potential biomarkers for early diagnosis, and targeted circuit interventions.

Editorial Notes:

  • This article was edited by a Neuroscience News editor.
  • Journal paper reviewed in full.
  • Additional context added by our staff.

About this neurology and brain aging research news

Author: Claire Turner
Source: PLOS
Contact: Claire Turner – PLOS
Image: The image is credited to Neuroscience News

Original Research: Open access.
Brain aging patterns among nine neurological disorders: A case-control study” by Chuang Liang, Godfrey Pearlson, Juan Bustillo, Peter Kochunov, Jiayu Chen, Xiangrong Zhang, Rongtao Jiang, Kent E. Hutchison, Jing Sui, Zening Fu, Xiao Yang, Yuhui Du, Daoqiang Zhang, Shile Qi, Vince D. Calhoun. PLOS Medicine
DOI:10.1371/journal.pmed.1004860

Northwell’s Phelps Hospital First in Westchester to Offer Vivistim Procedure for Stroke Recovery

  WOW, admitting COMPLETE FUCKING INCOMPETENCE in how long it took to bring vagus nerve stimulation into their stroke practice. And you haven't fired the board of directors for incompetence yet?

vagus nerve (67 posts to July 2012)

 And why not the non-surgical ones? Or do you need the surgical revenue?

Northwell’s Phelps Hospital First in Westchester to Offer Vivistim Procedure for Stroke Recovery

Cutting-edge neuro-rehabilitation technology helps chronic stroke survivors restore arm and hand function

Northwell’s Phelps Hospital has become the first hospital in Westchester County to offer the FDA-approved Vivistim® Paired VNS™ System, a revolutionary therapy for stroke rehabilitation. This innovative treatment provides new hope for chronic ischemic stroke survivors to regain upper limb function and improve quality of life.

Vivistim is an implantable device, similar to a pacemaker, that is placed in the upper chest and neck to deliver gentle electrical stimulation to the vagus nerve during targeted rehabilitation exercises. This unique "paired" approach is designed to help stroke survivors who have plateaued in traditional therapy relearn and improve motor skills in their affected arm and hand. The Vivistim System has been shown in clinical trials to achieve two to three times greater functional improvement than traditional rehabilitation therapy alone.

Call or click below to schedule an appointment.

"We are incredibly proud to be the first in Westchester to offer the Vivistim Paired VNS System," said Christian Ferreira, MD, cerebrovascular neurosurgeon at Phelps Hospital. "For patients who have struggled with persistent arm and hand weakness years after their stroke, this therapy offers renewed hope. It leverages the brain's natural ability to relearn — known as neuroplasticity — providing an opportunity for significant functional improvement that can profoundly impact their daily lives and independence."

This novel therapy combines rehabilitation with vagus nerve stimulation (VNS), a treatment that administers electrical impulses to the vagus nerve, one of the longest nerves in the body. Patients engage in activities ranging from simple tasks like brushing their teeth, writing or getting dressed to more complex daily routines such as preparing meals or playing games. The Vivistim device is activated during these exercises, helping strengthen the neural pathways responsible for movement and essential for regaining lost function.

Candidates for Vivistim are chronic ischemic stroke survivors, at least six months post-stroke, with moderate to severe upper limb deficits and have plateaued in their recovery.

“Bringing this advanced neuro-rehabilitation technology to Westchester underscores Phelps Hospital's unwavering commitment to delivering cutting-edge care and improving patient outcomes right here in our community,” said David Gordon, MD, chair of neurosurgery for Northwell in Westchester. “The introduction of Vivistim at Phelps provides local access to this life-changing therapy for stroke survivors throughout Westchester and the Hudson Valley, eliminating the need to travel outside the region for this specialized treatment.”

The addition of Vivistim builds on Northwell's continued investment in neurological care across the region, bringing the most advanced treatments closer to the communities it serves. Over the past year, the health system expanded its neurosurgical practice with a new dedicated location at Phelps Hospital and launched a $1.96 million comprehensive neurology practice in nearby Chappaqua Crossing.

Phelps provides the full spectrum of ischemic stroke care, from IV thrombolysis and mechanical thrombectomy to emergent neurosurgical procedures. The hospital has been designated a thrombectomy-capable stroke center by the Joint Commission, the American Heart Association (AHA) and the American Stroke Association (ASA). The AHA and ASA have also recognized Phelps with the Get With The Guidelines® Stroke Gold Performance Achievement Award, as well as the Target: Stroke Honor Roll - Elite and Target: Stroke Honor Roll for advanced therapies. 

6 simple exercises to help you live longer—no gym equipment needed

 Did your competent? doctor get you recovered enough to do these? NO? SO YOUR DOCTOR IS COMPLETELY FUCKING INCOMPETENT? There is no other choice!

6 simple exercises to help you live longer—no gym equipment needed

  • Dr. Wendolyn Gozansky, MD, geriatrician, vice president and chief quality officer at Kaiser Permanente Colorado
  • Dr. Mark Kovacs, PhD, FACSM, human performance scientist, longevity expert, and founder of the Kovacs Institute for Sport and Human Performance 
  • Jenny Liebl, certified personal trainer and senior content developer at ISSA (International Sports Sciences Association)

It’s no secret that physical activity is crucial for aging well. “One of the best ways to ensure a long healthspan—the time spent living free of major disease and disability—is to exercise regularly,” says geriatrician Dr. Wendolyn Gozansky, MD. However, this doesn’t mean you need to join a gym to enjoy the longevity-boosting effects of exercise. In fact, you don’t even need to leave the house. These are certain types of exercise that can help you live longer, so long as you do them consistently. Read on to learn about these moves, as explained by experts.

The Link Between Exercise and Longevity

While all exercise is beneficial for overall health and longevity, Dr. Gozansky says there are three types that are important for healthy aging: strength training, aerobics, and balance.

More specifically, these types of exercise address aspects of health that determine longevity and lifespan. “As we age, we must prioritize movements that preserve muscle mass, support cardiovascular function, [help] cognitive performance, and enhance neuromuscular coordination,” explains human performance scientist Dr. Mark Kovacs, PhD, FACSM. The good news? It’s possible to practice such movements at home with little to no equipment.

Best At-Home Exercises That Will Help You Live Longer

In addition to other lifestyle habits like prioritizing sleep, fostering social connections, and eating well, the following exercises can improve your overall lifespan. But remember: You don’t need to do these moves at a high-intensity level. Instead, it comes down to consistency and regular activity.

There are many health benefits of walking, and longevity is certainly on the list. Walking is a type of aerobic exercise that increases your heart rate and improves your cardiovascular health, Dr. Gozansky says. Walking is also a weight-bearing exercise, which will keep your bones strong, she adds. This is crucial because bone strength supports mobility and reduces the risk of fractures as you get older.

02 of 06

Step-Ups

If you want to take your aerobics game up a notch, try step-ups. You can do them on an exercise stepper or just step on a staircase. “Step-ups mimic real-life functional movements like stair climbing,” Dr. Kovacs says. “They improve aerobic capacity, single-leg balance, and joint stability—key for preventing falls and maintaining cardiovascular health.” You can do this exercise with your bodyweight, but if you’d like a challenge, add light weights or increase the speed, Dr. Kovacs suggests.

Squats

Squats build and maintain lower body strength, which is critical for fall prevention, mobility, and independence as we age,” Dr. Kovacs says. Plus, “they activate major muscle groups, enhance insulin sensitivity, and support bone density, especially in the hips and spine.” The best part: Squats are effective sans equipment, but you can challenge yourself by holding household items like paint cans, suggests certified personal trainer Jenny Liebl. Another option is to perform a squat hold hovering over a chair, which will build muscular endurance, Liebl suggests.

04 of 06

Modified Push-Ups

My problems:

  1.  Fingers and thumb will not stay flat due to spasticity.
  2. Wrist collapses.
  3. Elbow collapses.
  4. Bicep spasticity pulls everything out of line.
What is your doctors' protocol to get pushups done?  My doctor completely failed at this recovery and curing spasticity. Don't know why he was still employed there

“Push-ups build upper body strength and core stability while enhancing cardiovascular response in short bursts,” Dr. Kovacs explains. This is noteworthy because maintaining upper body strength is associated with lower all-cause mortality in midlife and older adults. However, these benefits aren’t limited to standard floor push-ups. You can enjoy the same benefits by doing push-ups with your hands on a wall or countertop, Dr. Kovacs says. As you get stronger, try floor push-ups on your knees, then progress to full push-ups.

Single-Leg Stands

On my good leg I can do this, my bad leg not even close. Since I haven't been able to do this since my stroke at age 50 I guess I should have died sometime in the ensuing 20 years. I thought the Berg Balance Scale testing  that was common, was totally worthless since there never was any specific therapy given to address the failure points I had in that test. So 20 years of failure already and my next 30 years will be no better, totally useless for me!

Single-leg stands are another at-home exercise that can help you live longer. It’s a type of balancing exercise, which, when done regularly, can help prevent falls, the leading cause of death from injury in adults 65 years and older, Dr. Gozansky says. “Consider doing this activity whenever you’re near a sturdy countertop, [like] in the bathroom before brushing your teeth or at the kitchen sink before washing the dishes,” Dr. Gozansky suggests. Eventually, try single-leg stands without support to further improve balance.

06 of 06

Plank Holds

At first glance, the plank might look like an uneventful exercise. But according to Dr. Kovacs, it’s beneficial for longevity. Planks activate “deep stabilizer muscles, improve neuromuscular coordination, and support spinal integrity, [which] are all essential for daily movement and fall resistance,” he says. Together, these factors enhance physical function (and ultimately, independence) in later years. If a standard plank feels too difficult, remember that you can modify it by dropping your knees to the ground.

Read the original article on Real Simple

More failed hospitals promoting their 'care' rather than their recovery statistics! Don't go there!

 If everyone in your hospital can't immediately tell you these three statistics THEY ARE A COMPLETE FUCKING FAILURE! It means they aren't measuring anything at all! You can't measure 'care'. They should be in neon lights over the front entry desk!

There is no quality here if you don't measure the right things. Is your incompetent? hospital even measuring these?

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

Here is your business101 requirements. Not measuring 100% recovery is the height of incompetence!

“What's measured, improves.” So said management legend and author Peter F. Drucker !   

The latest here:

 UHS earns national recognition for excellence in stroke care for third consecutive year 

Stony Brook Eastern Long Island Hospital earns national stroke care award 

HCA Florida Lehigh Hospital Awarded Primary Stroke Certification from Joint Commission 

Hendrick Health wins national awards for cardiac care - Abilene Reporter-News 

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This Russian Peptide Regrew Brain Cells in Stroke Rats. The Human Data Is Thin But the Safety Record Spans 3 Decades

 Three decades of incompetence in your doctor and hospital in not getting this to an interventional protocol! Aren't you glad of WORLD CLASS INCOMPETENCE in your facility?

 Of course your competent? doctor already has EXACT PROTOCOLS that deliver all the BDNF you need. And has been for over a decade, right? But your doctor incompetently knew nothing and did nothing, right? Which means your board of directors is so incompetent they can't recognize incompetence in their staff!

  • BDNF (209 posts to April 2011)

This Russian Peptide Regrew Brain Cells in Stroke Rats. The Human Data Is Thin But the Safety Record Spans 3 Decades

A clear pill that lets you read a book in 15 minutes and actually remember it. Learn Italian over a weekend. Use that new skill to charm an Italian supermodel you can now understand both literally and emotionally.That’s the pitch of the movie Limitless, where Bradley Cooper transforms from washed-up writer to Wall Street genius after taking a designer drug.Society has chased chemical brain boosters for over a century. World War II literally ran on speed—Germans had Pervitin (methamphetamine they nicknamed “tank chocolate”), while Allies distributed Benzedrine, basically 1940s Adderall.

The Air Force fed pilots “go pills”—pure dextroamphetamine—from Vietnam through Afghanistan, which may have contributed to a 2002 incident where two US pilots on Dexedrine accidentally bombed a Canadian unit.

The pattern never changes: every shortcut works, but every shortcut bills you—whether it’s your heart, sleep, or addiction risk.

Enter Soviet Neuroscience

Semax is a heptapeptide—seven amino acids strung together: methionine, glutamate, histidine, phenylalanine, proline, glycine, and proline.

Unlike other peptides extracted from animal tissue, Semax was designed on purpose by Soviet pharmacologists at Moscow’s Institute of Molecular Genetics starting in the 1980s.

Researchers started with a fragment of ACTH (adrenocorticotropic hormone), which normally tells adrenal glands to produce cortisol. A four-amino-acid fragment showed positive stress effects on brain function—think learning, attention, resistance to low oxygen—without hormonal downsides like muscle breakdown.

Scientists welded on a proline-glycine-proline tail to prevent enzymatic degradation, creating a brain-targeted stress hormone fragment with built-in stabilizer. A non-stimulant cognitive booster with no obvious addiction profile—exactly what everyone had been hunting for.

At roughly 814 daltons, Semax is relatively small (BPC-157 is about 1,419, semaglutide exceeds 4,000). Small enough that Russians believed nasal mucous membranes could deliver it directly to brain tissue—hence the nasal drop delivery method.

How Semax Actually Works

The headline mechanism involves BDNF—brain-derived neurotrophic factor. Think of it as fertilizer for neurons, helping them survive, connect, and rewire.

In rat studies, Semax increases BDNF and its receptor TrkB in hippocampus and forebrain. That’s the most coherent thread in Semax research and the basis for every neuroplasticity claim attached to it.

It also nudges monoamine neurotransmitters like dopamine and serotonin. But here’s critical nuance matching user reports: Semax is not a stimulant.

In rat studies, Semax alone barely moved dopamine but amplified response when something else was already driving it. That’s why most users describe feeling more motivation rather than a true buzz.

It’s Not NZT

The entire Limitless premise builds on the myth that we only use a fraction of our brains. Unfortunately, that’s fiction—we’re already using essentially 100% of our brains at baseline.

Semax doesn’t unlock dormant capacity waiting for activation. It optimizes signaling in tissue you’re already running.

What Does Science Actually Show

The evidence is present but lopsided in a very specific way.

Bench and animal data is surprisingly deep. Cell studies show BDNF and nerve growth factor genes activating. Rat stroke research is strongest—researchers literally tied off brain arteries in rats, administered Semax, then watched gene expression shift from inflammatory/injury patterns toward repair.

One study showed boosted cell proliferation in injured rat brains, spawning online claims that “Semax regrows your brain.” But again, this is in mice—not 35-year-old humans trying to focus on Excel spreadsheets.

Human Data Is Thin and Russian

A small fMRI study showed intranasal Semax measurably changed brain network activity in healthy volunteers. Older EEG and cognitive work from the 1990s exists, plus a stroke rehab study where Semax plus early rehabilitation raised blood BDNF and slightly accelerated recovery.

But large placebo-controlled trials examining cognitive improvements—how most people actually use it—are still lacking.

Russia has used Semax as an approved drug for over 30 years in stroke patients, giving it more real-world data than almost any non-FDA-approved substance. While not as robust as semaglutide trials, in some ways it’s better—GLP-1 agonists haven’t been around nearly as long.

Semax’s efficacy as cognitive booster may be fuzzy, but its safety profile appears solid.

Dosing: Russian Medicine vs. Gray Market

Russian pharmaceutical Semax comes as nasal drops in two strengths: 0.1% solution for cognitive boost and stroke recovery, and stronger 1% reserved for acute hospital stroke treatment.

One drop of 0.1% delivers approximately 50 micrograms. Labeled daily range runs from a few hundred up to couple thousand micrograms, usually for only a few days at a time.

Gray market biohackers report using nasal sprays between 100-1,000 micrograms daily, typically 5 days on, 2 days off, because tolerance develops quickly and spray isn’t cheap.

Some insist they get better results from subcutaneous injection, though this has no obvious upside and adds another needle to weekly routine.

The Gray Market Problem

When buying “research use only” Semax, there’s decent chance you’re not buying Semax itself. There’s an entire family of remixes: N-acetyl Semax and N-acetyl Semax amidate (Adamax), each with chemical tweaks to extend half-life or intensify effects.

Those aren’t the molecules from Russian studies. Your mileage may vary—like buying a live bootleg concert recording where maybe it sounds better than studio version, or maybe the artist is drunk and slurring.

Side Effects and Safety

Semax is generally well-tolerated, which is major part of its appeal. But well-tolerated doesn’t mean risk-free.

Common user-reported complaints include:

  • Anxiety and irritability
  • Headaches
  • Nausea
  • Insomnia if taken late in day
  • Unpleasant emotional intensity—like volume got cranked on whatever you were already feeling

The single most common complaint? Feeling absolutely nothing, even at high doses. Could mean bad product, incomplete absorption, wrong analog, or simply individual non-response.

Russian labeling contraindicates pregnancy, breastfeeding, acute psychiatric illness, and notably, history of seizures. Anything nudging brain excitability deserves respect—”naturally derived peptide” doesn’t automatically mean benign.

The scariest thing about Semax in the USA isn’t the peptide itself—it’s the bottle. Since it can’t be legally manufactured here for human consumption, there’s zero guarantee regarding purity, sterility, or whether labeled dose matches actual contents.

FDA Meeting Could Change Everything

On July 23-24, the FDA’s Pharmacy Compounding Advisory Committee (PCAC) meets to decide the fate of several peptides, including Semax.

BPC-157, KPV, TB-500, and MOTS-c are up day one. Semax joins Epitalon and Dihexa on day two, July 24th.

These peptides exist in regulatory limbo. This meeting decides whether they return to a list allowing compounding pharmacies to legally manufacture them under real oversight with quality control, or stay banished to gray market forever.

For Semax specifically, the committee reviews it for cerebral ischemia and trigeminal neuralgia. While PCAC votes are technically advisory, FDA won’t grant access to legitimate high-quality Semax from compounding pharmacies without it.

There’s a public comment docket at regulations.gov that committee members must consider. Comments submitted by July 9th get physically handed to committee before the meeting. After that deadline, FDA may still read them, but people casting votes won’t see them.

The Real Limitless Pill

Is Semax a real-life limitless pill? Probably not. We’re still waiting for actual NZT, and nothing flips your brain to 100% because you’re already running at 100%.

Remember how Limitless actually ends: even fictional NZT had a body count—tolerance, blackouts, withdrawal, people dying when supply runs dry. Even the fantasy came with a bill.

But is Semax a real molecule with genuine cognitive effects, legitimate neuroprotective properties, and 30 years of Russian clinical use? Absolutely. It emerged from legitimate pharmaceutical research in Moscow, not a Hollywood writer’s room.

Semax may be subtle and context-dependent, but positive signals appear exactly where they matter—in cognition and the injured, stressed brain.

Your Real NZT Already Exists

For those chasing focus, the closest thing to a real-life limitless pill is less exciting than movie trailers but costs nothing: sleep, blood pressure control, exercise, avoiding alcohol, treating sleep apnea, addressing depression.

That’s your NZT. Once those fundamentals are dialed, Semax might be reasonable value-add. But it isn’t the whole meal.

When fundamentals are out of whack, nothing else does the work for you. The fanciest Russian nasal spray on Earth will likely be one big expensive disappointment.

Semax is a real molecule with real effects and genuine potential—but it’s a tool, not magic. And if you want access to properly manufactured versions with quality control, make your voice heard at the FDA docket before July 9th.