Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,278 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.
ZFP384 inhibition prolonged brain repair and improved recovery in stroke models.
Blocking the activity of ZFP384 can prolong the brain’s endogenous repair functions after stroke, report researchers in a collaborative study. They developed an antisense oligonucleotide-based therapy that sustained the reparative activity of microglia by promoting remyelination and neural plasticity, thereby improving functional recovery in mice. Surprisingly, these results were observed even when the treatment began weeks after injury. The findings reveal a promising strategy to extend the brain’s recovery window after stroke, improving long-term outcomes.
Stroke is one of the leading causes of long-term disability worldwide, which often results in impairments in movement, speech, and cognition in patients. While rehabilitation helps patients regain some lost functions, the brain’s natural ability to repair itself often fades within a few months after an injury. This limited period of spontaneous recovery poses a major challenge for patients, often resulting in permanent neurological deficits after the brain’s intrinsic repair capacity declines. Although this loss of reparative ability has been studied extensively, the mechanism behind this loss remains unclear.
To uncover the reason why this happens, a team led by Assistant Professor Jun Tsuyama and Professor Takashi Shichita from the Department of Neuroinflammation and Repair, Institute of Science Tokyo (Science Tokyo), Japan, conducted research in collaboration with researchers from the Tokyo Metropolitan Institute of Medical Science, Kyushu University, Japan, and the University of Freiburg, Germany. Their findings were published in the journal Nature on May 13, 2026.
After a stroke, the brain launches a coordinated repair program that involves several types of cells. Among these, microglia, the brain’s resident immune cells, play a pivotal role. Immediately after an injury, microglia are activated to trigger inflammation, but thereafter, they rapidly transition into a reparative state and produce growth factors, such as insulin-like growth factor 1 (IGF1), which support remyelination, strengthen neural connections, and promote functional recovery. But this only lasts for two months, limiting the brain’s capacity to repair further.
Tokyo, May 14 (Jiji Press)--A team including Takashi Shichita, a professor at the Institute of Science Tokyo's Medical Research Laboratory, has developed a drug candidate to suppress a type of protein that causes the rehabilitation-induced partial recovery of motor functions lost from a stroke to end after only about two months.
People who lost the abilities to move their hands or feet, or to speak due to the deaths of some nerve cells in their brains from the cerebral infarction can regain the functions to a certain extent through rehabilitation. The recovery normally lasts for about two months.
The recovery is possible because surviving nerve cells repair the neuron networks, with microglia, or cells in charge of brain immunity, helping the restoration process by secreting a protein called insulin-like growth factor 1, or IGF1.
In a genetic manipulation experiment using mice, Shichita and other members of the team discovered that microglia stopped secreting IGF1 after a while following a stroke due to the function of another protein, ZFP384. The same mechanism was confirmed in the brains of dead stroke patients.
The team developed the drug candidate to block the production of ZFP384. After injecting the drug into mice, the team found that microglia continued to secrete IGF1 and helped maintain the recovery of brain functions.
(This is an excerpt of the Health Rounds newsletter, where we present latest medical studies on Tuesdays and Thursdays)
By Nancy Lapid
Dec 3 (Reuters) - Stroke patients who can't get to the hospital quickly enough to be eligible for the usual clot-busting treatments may soon have another option, results from a mid-stage trial suggest.
Currently available thrombolytic drugs must be given within a few hours after symptoms begin. That narrow window can rule out patients who did not, or could not, seek help promptly because they didn’t immediately recognize their symptoms, as well as those who wake up with symptoms of a stroke that may have started hours earlier.
The experimental drug being developed by Silver Creek Pharmaceuticals and dubbed scp776 inhibits apoptosis, a process in which injured cells self-destruct.
The drug keeps injured cells alive by delivering a hormone called insulin-like growth factor 1, or IGF-1, which activates the cells’ natural repair pathways.
In 119 patients who came to emergency departments on average about 12 hours after stroke onset - for whom there was no approved drug treatment - scp776 resulted in clinically meaningful improvements in outcomes compared to a placebo, researchers reported at the 2025 World Stroke Congress in Barcelona.
“It’s very promising to see a therapy that leverages the brain’s own recovery mechanisms to improve stroke outcomes in the clinic,” Silver Creek Chief Scientific Officer Kris Kuchenbecker said in a statement.
At the time of hospital discharge, or by day 7 after symptom onset, patients receiving scp776 had on average a clinically significant 2.26-point higher score on the 42-point NIH Stroke Scale compared to those who received a placebo, although the difference was just short of statistical significance.
At 90 days, the treatment had resulted in a 15% increase in the relative proportion of patients achieving functional independence, researchers reported.
The drug has received FDA Fast Track designation for acute ischemic strokes caused by blockages in the arteries that carry blood to the brain. The Food and Drug Administration awards the designation to speed development and review of treatments for serious conditions where there is an unmet need.
“Scp776 harnesses the well-understood repair power of growth factors in a targeted way, finally delivering on the vast preclinical evidence of therapeutic benefit of IGF-1,” Kuchenbecker said.
AI IMPROVES SCREENING FOR FETAL HEART PROBLEMS
Artificial intelligence software can improve fetal screening for congenital heart defects, according to results of a new study.
Using a tool from medical company BrightHeart, researchers analyzed 200 fetal ultrasound scans obtained during the second trimester of pregnancy from women at 11 medical centers in two countries, including 100 with at least one suspicious finding.
Seven obstetrician-gynecologists and seven doctors who specialize in high-risk pregnancies reviewed each examination in randomized order, both with and without AI assistance, looking for findings that might indicate the presence of a severe heart defect.
The physicians detected more suspicious lesions, and in less time, with AI than without, according to a report in Obstetrics & Gynecology.
Overall, their detection rate rose from 82% to more than 97%, with an 18% reduction in reading time and 19% improvement in confidence scores.
“Our study should prompt and encourage future research into AI-assisted software's ability to improve detection rates... (and) reduce the variability and inequity of detection of congenital heart defects globally,” study co-leader Dr. Andrei Rebarber of the Icahn School of Medicine at Mount Sinai said in a statement.
“The future for prenatal diagnostic imaging is bright when AI software is employed as an adjunct to physician interpretation.”
(To receive the full newsletter in your inbox for free sign up here)
(Reporting by Nancy Lapid; Editing by Bill Berkrot)
Your competent? doctor is responsible for initiating research into delivering these to stroke patient brains! If your doctor doesn't do that; YOU DON'T HAVE A FUNCTIONING STROKE DOCTOR! RUN AWAY!
Neurodegenerative brain diseases such as
Alzheimer’s disease (AD), multiple sclerosis (MS), and Parkinson’s
disease (PD) are difficult to treat. Unfortunately, many therapeutic
agents for neurodegenerative disease only halt the progression of these
diseases and do not reverse neuronal damage. There is a demand for
finding solutions to reverse neuronal damage in the central nervous
system (CNS) of patients with neurodegenerative brain diseases.
Therefore, the purpose of this review is to discuss the potential for
therapeutic agents like specific neurotrophic and growth factors in
promoting CNS neuroregeneration in brain diseases. We discuss how BDNF,
NGF, IGF-1, and LIF could potentially be used for the treatment of brain
diseases. The molecule’s different mechanisms of action in stimulating
neuroregeneration and methods to analyze their efficacy are described.
Methods that can be utilized to deliver these proteins to the brain are
also discussed.
Since I'm sure your competent? doctor completely failed at getting you 100% recovered so that you can't get the full benefits of exercise for neuroplasticity, WHAT EXACTLY IS YOUR DOCTOR DOING WITH THESE MIMETICS? Nothing, like usual?
Exercise mimetic is a new strategy for neurological disorders by boosting neurogenesis
There is an increasing consensus on the positive effects of physical exercise in a broad spectrum of models of human diseases [148, 149], particularly CNS disorders such as AD and PD [150].
Besides the therapeutic effects on the pathological process of
diseases, exercise also has a favourable impact on cognitive function in
neurodegenerative disorders [6, 8, 33, 151, 152]. It is fairly clear, as many studies have discussed [38, 153, 154],
that exercise could be developed as a pharmacological strategy for
neurodegeneration and cognitive dysfunction, presenting as exercise
mimetics [38, 39, 155] (Table 1).
This becomes particularly important for older adults and patients with
injuries or severe neurological diseases who have difficulties in
conducting exercise regimens. Exercise mimetics are an attempt to let
‘exercise effects’ become available to the whole population through
pharmacological proteins or factors (such as BDNF, Clusterin, irisin,
and IGF-1) (Table 1).
Interestingly, several featured studies have been conducted recently to
explore the potential of ‘exercise mimetics’ in improving brain
functions in neuropathological or ageing conditions [34, 36, 37].
Understanding the molecular and cellular processes underlying the
communications between the periphery and the brain (such as muscle-brain
crosstalk, liver-brain axis, and gut-brain axis) in response to
exercise can facilitate development of exercise mimetics. We here
particularly focus on the molecular effects of exercise mimetics on
adult neurogenesis and cognitive function in neurological disorders.
Table 1 Candidate molecules of exercise mimetics for the treatment of neurodegenerative disorders
I hate treadmills, they do nothing for balance recovery and fall prevention, and are boring as hell. So it is your doctor's responsibility to give you EXACT EXERCISES TO DO!
In a recent article published in Experimental Gerontology,
researchers systematically reviewed English language publications from
13 electronic databases, such as PubMed/Medline, Google Scholar, and Web
of Science.
They investigated which exercises might enhance anti-inflammatory
cytokines and reduce pro-inflammatory cytokines in patients with
dementia or mild cognitive impairment (MCI), as illustrated in studies
using apt animal models and human participants.
Background
MCI is often considered the earliest symptomatic manifestation of
Alzheimer's disease (AD), the most common cause of dementia. By 2050, AD
might become so prevalent that one in 85 people will have AD worldwide.
Cognitive deficits, neurodegeneration, b-amyloid (Aβ) deposition,
neurofibrillary tangle (NFT) formation, and neuroinflammation are some
of the characteristic manifestations of AD.
There is a need for biomarker panels to diagnose AD early. Their
identification is also crucial because inflammatory mediators play an
important role in disease pathogenesis and could inform the development
of novel therapeutic strategies for AD.
About the study
In the present study, researchers performed a detailed systematic
review to understand the effects of chronic physical activity on MCI or
AD outcomes. They included studies using exercise, physical activity, or
fitness training as an experimental intervention.
These articles had participants who either had AD, MCI, or dementia,
examined cerebrospinal fluid (CSF), brain tissue, etc., and measured
cytokines or other inflammatory or neuroinflammatory immune markers. The
researchers also included all animal studies that responded to these
criteria.
In the study assessments, the researchers examined the effect of
physical activity, stratified based on its type, frequency, volume,
intensity, and duration.
Results
The authors claim this is the first systematic study on physical
exercise parameters in this context. Thus, the studies covered in this
review showed inflammatory and anti-inflammatory cytokine levels after
exercise in the intervention and control groups.
The included studies also combined results from 25, 11, and two
articles exclusively related to animals, humans, and both humans and
animals, respectively. They include 1249 animals and 789 human
participants.
First,
the researchers evaluated only animal model articles to find that
physical exercise reduced pro-inflammatory markers in 70.8% of the
models, especially tumor necrosis factor-alpha (TNF-α), interleukin
(IL)-1β, and IL-6. In 26% of the animal model articles, the levels of
the anti-inflammatory cytokines, viz., IL -4, IL -4β, IL -10β, IL -10,
and TGF-β showed a marked increase.
In 40.8% of animal model studies, the effect on cytokine levels was
positive post-treadmill and swimming exercises, whereas resistance
exercise decreased pro-inflammatory cytokines. These three exercise
types also promoted a marked reduction in Aβ amyloid plaques,
pro-inflammatory cytokines, and microglial activation. Further, the
researchers noted elevated levels of IL -4 after four weeks of exercise,
through which the brain most likely compensated for Aß-induced
upregulation of IL-6.
A low, moderate, or high treadmill exercise volume decreased IL -1β
and a surge in anti-inflammatory cytokine IL -10 in blood serum.
Furthermore, the study results showed that low-intensity endurance
training reversed neuroinflammation.
Intriguingly, 73% of studies where authors induced AD in
non-transgenic animals found a positive exercise effect on
neuroinflammation. In 100% of articles, hippocampal Aβ injection was
very effective concerning neuroinflammation.
Moving on to studies with human models, the researchers observed that
chronic exercise was beneficial. In 53.9% and 23% of chronic exercise
articles, they observed reduced pro-inflammatory and increased
anti-inflammatory cytokines, respectively.
Accordingly, cycling, aerobic and multimodal exercises, and
resistance training reduced several pro-inflammatory cytokines, e.g., IL
-6, IL -15, IL -1β, and TNF-α. Even in older adults with MCI, three
times per week of multimodal training for 16 weeks reduced blood serum
levels of IL -6 and TNF-α.
Likewise, resistance training had multiple benefits. For instance, it
improved their cognitive function by increasing insulin-like Growth
Factor One (IGF-1) levels in the hippocampus. Similarly, aerobic and
mind-plus-body exercises increased Brain-derived neurotrophic factor
(BDNF), whereas cycling reduced small nucleolar RNA host gene 14
(SNHG14) expression to halt AD progression.
Conclusions
The authors emphasized that future studies elucidate the effect of
exercise protocols on AD stages, from preclinical to severe. Similarly,
understanding the correlation between cytokine levels and cognitive
functions is crucial to managing neuroinflammation and cognitive
decline.
Furthermore, future studies should have a larger sample size covering
both genders where they compare groups doing two different types of
exercise, rather than a sedentary group vs. an exercise group. It would
enhance understanding of how forced physical activity accentuates
dementia progression.
Nonetheless, this review remarkably showed the positive effects of
chronic physical activity on the brain tissue of animals and humans with
MCI or AD. Though the study results could help guide healthcare
professionals, the authors cautioned that this efficacy was biological and not proven clinically.
Just talked to my doctor today about metformin, she said it's too early to tell, no clinical studies have been run on it yet. And since I'm not even pre-diabetic, I can't wheedle my way onto the drug.
You'll have to read about dietary restriction in this book: '
Tackling the mechanisms underlying ageing is desirable to help to extend the duration
and improve the quality of life. Life extension has been achieved in animal models
by suppressing the growth hormone–insulin-like growth factor 1 (IGF-1) axis and also
via dietary restriction. Metformin has become the focus of increased interest as a
possible anti-ageing drug. There is some overlap in the postulated mechanisms of how
these three approaches could produce anti-ageing effects, with convergence on common
downstream pathways. In this Review, we draw on evidence from both animal models and
human studies to assess the effects of suppression of the growth hormone–IGF-1 axis,
dietary restriction, and metformin on ageing.
William S. Dodd,1 Eric J. Panther,1 Kevin Pierre,1
Jairo S. Hernandez,1 Devan Patel,2 Brandon LuckeWold1,*
1. Department of Neurosurgery, College of Medicine, University of Florida, Gainesville, FL
2. Department of Neurosurgery, Jacobs School of Medicine and Biomedical Sciences, University at
Buffalo, Buffalo, NY
* Correspondence to:
Brandon Lucke-Wold, MD, PhhD
Lillian S. Wells Department of Neurosurgery
1505 SW Archer Rd
Gainesville, FL 32608
brandon.lucke-wold@neurosurgery.ufl.edu
Abstract
Traumatic brain injury (TBI) is a devastating event with severe long-term complications. TBI and
its sequelae are one of the leading causes of death and disability in those under 50 years old. The full
extent of secondary brain injury is still being intensely investigated; however, it is now clear that
neurotrauma can incite chronic neurodegenerative processes. Chronic traumatic encephalopathy,
Parkinson’s disease, and many other neurodegenerative syndromes have all been associated with a
history of traumatic brain injury. The complex nature of these pathologies can make clinical assessment,
diagnosis, and treatment challenging. The goal of this review is to provide a concise appraisal of the
literature with focus on emerging strategies to improve clinical outcomes. First, we review the pathways
involved in the pathogenesis of neurotrauma-related neurodegeneration and discuss the clinical
implications of this rapidly evolving field. Next, because clinical evaluation and neuroimaging are
essential to the diagnosis and management of neurodegenerative diseases, we analyze the clinical
investigations that are transforming these areas of research. Finally, we briefly review some of the
preclinical therapies that have shown the most promise in improving outcomes after neurotrauma
Study tested acute effects of exercise intensity on circulating
molecules related to neuroplasticity, including vascular-endothelial
growth factor (VEGF), insulin-like growth factor-1 (IGF1), and cortisol,
using the same data set and serum samples as a previous brain-derived
neurotrophic factor (BDNF) analysis. Sixteen participants with chronic
stroke performed 3 exercise protocols in random order: treadmill
high-intensity interval training (HIT-treadmill), seated-stepper HIT
(HIT-stepper), and treadmill moderate-intensity continuous exercise
(MCT-treadmill). Serum molecular changes were compared between
protocols. Mediation and effect modification analyses were also
performed. VEGF significantly increased during HIT-treadmill, IGF1
increased during both HIT protocols and cortisol nonsignificantly
decreased during each protocol. VEGF response was significantly greater
for HIT-treadmill versus MCT-treadmill when controlling for baseline.
Blood lactate positively mediated the effect of HIT on BDNF and
cortisol. Peak treadmill speed positively mediated effects on BDNF and
VEGF. Participants with comfortable gait speed ≥0.4 meters per second
had significantly lower VEGF and higher IGF1 responses, with a lower
cortisol response during MCT-treadmill. BDNF and VEGF are promising
serum molecules to include in future studies testing intensity-dependent
mechanisms of exercise on neurologic recovery. Fast training speed and
anaerobic intensity appear to be critical ingredients for eliciting
these molecular responses. Serum molecular response differences between
gait speed subgroups provide a possible biologic basis for previously
observed differences in training responsiveness. Descriptor Terms: BIOCHEMISTRY, EXERCISE, MOBILITY IMPAIRMENTS, OUTCOMES, STROKE, THERAPEUTIC TRAINING.
So where is the protocol that specifies EXACTLY HOW MUCH BDNF WE NEED FOR RECOVERY? AND THEN THE EXACT AMOUNT OF EXERCISE TO PRODUCE THAT? That is what effective stroke leadership would demand be produced.
Background.
Exercise intensity can influence functional recovery after stroke, but the mechanisms remain poorly understood. Objective.
In chronic stroke, an intensity-dependent increase in circulating
brain-derived neurotrophic factor (BDNF) was previously found during
vigorous exercise. Using the same serum samples, this study tested acute
effects of exercise intensity on other circulating molecules related to
neuroplasticity, including vascular-endothelial growth factor (VEGF),
insulin-like growth factor-1 (IGF1), and cortisol, with some updated
analyses involving BDNF. Methods.
Using a repeated-measures
design, 16 participants with chronic stroke performed 3 exercise
protocols in random order: treadmill high-intensity interval training
(HIT-treadmill), seated-stepper HIT (HIT-stepper), and treadmill
moderate-intensity continuous exercise (MCT-treadmill). Serum molecular
changes were compared between protocols. Mediation and effect
modification analyses were also performed. Results.
VEGF
significantly increased during HIT-treadmill, IGF1 increased during both
HIT protocols and cortisol nonsignificantly decreased during each
protocol. VEGF response was significantly greater for HIT-treadmill
versus MCT-treadmill when controlling for baseline. Blood lactate
positively mediated the effect of HIT on BDNF and cortisol. Peak
treadmill speed positively mediated effects on BDNF and VEGF.
Participants with comfortable gait speed ≥0.4 m/s had significantly
lower VEGF and higher IGF1 responses, with a lower cortisol response
during MCT-treadmill. Conclusions.
BDNF and VEGF are promising
serum molecules to include in future studies testing intensity-dependent
mechanisms of exercise on neurologic recovery. Fast training speed and
anaerobic intensity appear to be critical ingredients for eliciting
these molecular responses. Serum molecular response differences between
gait speed subgroups provide a possible biologic basis for previously
observed differences in training responsiveness.
1Department of Experimental Pharmacology, Center for Neurosciences (C4N), Vrije Universiteit Brussel, Brussels, Belgium
2Department of Neuroscience, University Medical Center Groningen, University of Groningen, Groningen, Netherlands
Post-stroke systemic injections of insulin-like growth factor-1
(IGF-1) exert neuroprotective effects in rats. In the current study, we
aimed to test the efficacy of IGF-1 neuroprotection in aged rats (24–25
months old) and to compare the results with adult rats (6–7 months old).
Furthermore, we addressed putative differences in microglial responses
to IGF-1 in adult and aged rats. Rats were subjected to ischemic stroke
while they were conscious by infusing endothelin-1 (Et-1) through a
guide cannula that was implemented in the vicinity of the middle
cerebral artery (MCA). Rats were given subcutaneous injections of IGF-1
(1 mg/kg) at 30 min and 120 min after the insult. Post-stroke IGF-1
treatment reduced the infarct size by 34% and 38% in aged and adult
rats, respectively. The IGF-1 treated adult rats also showed significant
improvement in sensorimotor function following stroke, while this
function was not significantly affected in aged rats. Furthermore, aged
rats displayed exaggerated activation of microglia in the ischemic
hemisphere. Significant reduction of microglial activation by IGF-1 was
only detected at specific regions in the ipsilateral hemisphere of adult
rats. We show that IGF-1 reduced infarct size in aged rats with an
ischemic stroke. It remains to be established, however, whether the
age-related changes in microglial function affect the improvement in
behavioral outcomes.
Introduction
Ischemic stroke is one of the most common causes of death and disability (Katan and Luft, 2018). Thrombolytic therapy with recombinant tissue plasminogen activator is still the most effective therapy for ischemic stroke (Lees et al., 2016; Alberts, 2017). However, many patients are not eligible for this therapy due to the narrow therapeutic window (Lees et al., 2016; Alberts, 2017).
Moreover, post-stroke treatment with systemically
injected IGF-1 induced neuroprotection in several rat models for
ischemic stroke (Rizk et al., 2007; De Geyter et al., 2013, 2016; Bake et al., 2014). These observations indicate that IGF-1 may be effectively used as a neuroprotective agent in patients.
Many preclinical studies successfully identified
neuroprotective drugs against ischemic stroke, but these drugs failed to
exert significant effects in the clinic (Green, 2008; Veltkamp and Gill, 2016). One of the recommendations of the Stroke Therapy Academic Industry Roundtable (STAIR; Fisher et al., 2009)
to facilitate translation to the clinic, is to include comorbidity
factors such as aging in preclinical studies. Indeed, the incidence of
stroke is higher in the elderly (Béjot et al., 2016).
Therefore, we tested whether IGF-1 treatment is neuroprotective in aged
rats and compared the results to the efficacy of IGF-1 in adult rats.
Preliminary experiments in our laboratory revealed that neuroprotection
by IGF-1 in rats with ischemic stroke is accompanied by microglial
changes and a decrease in neuroinflammation. Since age correlates with
an exaggerated activational state of microglia (Godbout et al., 2005; Norden and Godbout, 2013), we addressed the effects of IGF-1 on microglial activation.
Ahmad Serhan
Erik Boddeke
Ron Kooijman
