Use the labels in the right column to find what you want. Or you can go thru them one by one, there are only 34,483 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.
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 8, 2026
Psilocybin reduces fear memory and restores neuroplasticity in the hippocampus and medial prefrontal cortex
Saturday, May 4, 2024
Enhancing Neurogenesis for Parkinson’s Treatment
I'm assuming this means these new neurons are not generated in the hippocampus and thus do not need to be migrated to the proper location. Which means our stroke researchers(With any functioning brain cells at all) could figure out how to duplicate this for each type of neuron that was dead or damaged in your stroke! But that won't occur; there is NO STROKE LEADERSHIP THAT CAN GET STROKE SOLUTIONS ACCOMPLISHED!
Enhancing Neurogenesis for Parkinson’s Treatment
Summary: Researchers have pioneered a method to enhance the generation of dopaminergic neurons, crucial for Parkinson’s disease treatment, by targeting specific receptors within the Wnt signaling pathway. Using synthetic antibodies, the team successfully directed stem cell differentiation in the midbrain to produce these key neurons, which are instrumental in brain health and depleted in Parkinson’s patients.
This new approach could lead to more effective treatments for the disease, bypassing previous methods that caused unintended effects. Promising early results in rodent models show potential for restoring motor function, setting the stage for further preclinical tests.
Key Facts:
- Innovative Targeting Method: The researchers developed synthetic antibodies to selectively activate the FZD5 receptor in the Wnt signaling pathway, improving the precision of stem cell differentiation into dopaminergic neurons.
- Promising Preclinical Results: The neurons generated through this new method closely resemble natural dopaminergic neurons and have shown potential in alleviating symptoms of Parkinson’s in rodent models.
- Potential for Clinical Application: This study opens new avenues for developing Parkinson’s treatments that are more efficient and have fewer side effects, advancing closer to clinical trials.
Source: University of Toronto
Researchers at the University of Toronto have found a way to better control the preclinical generation of key neurons depleted in Parkinson’s disease, pointing toward a new approach for a disease with no cure and few effective treatments.
The researchers used an antibody to selectively activate a receptor in a molecular signaling pathway to develop dopaminergic neurons. These neurons produce dopamine, a neurotransmitter critical to brain health.
Researchers around the world have been working to coax stem cells to differentiate into dopaminergic neurons, to replace those lost in patients living with Parkinson’s disease. But efforts have been hindered in part by an inability to target specific receptors and areas of the brain.
“We used synthetic antibodies that we had previously developed to target the Wnt signaling pathway,” said Stephane Angers, principal investigator on the study and director of the Donnelly Centre for Cellular and Molecular Biology.
“We can selectively activate this pathway to direct stem cells in the midbrain to develop into neurons by targeting specific receptors in the pathway,” said Angers, who is also a professor in the Leslie Dan Faculty of Pharmacy and the Temerty Faculty of Medicine, and holds the Charles H. Best Chair of Medical Research at U of T. “This activation method has not been explored before.”
The study was recently published in the journal Development.
Parkinson’s disease is the second-most common neurological disorder after Alzheimer’s, affecting over 100,000 Canadians. It particularly impacts older men, progressively impairing movement and causing pain as well as sleep and mental health issues.
Most previous research efforts to activate the Wnt signaling pathway have relied on a GSK3 enzyme inhibitor. This method involves multiple signaling pathways for stem cell proliferation and differentiation, which can lead to unintended effects on the newly produced neurons and activation of off-target cells.
“We developed an efficient method for stimulating stem cell differentiation to produce neural cells in the midbrain,” said Andy Yang, first author on the study and a PhD student at the Donnelly Centre.
“Moreover, cells activated via the FZD5 receptor closely resemble dopaminergic neurons of natural origin.”
Another promising finding of the study was that implanting the artificially-produced neurons in a rodent model with Parkinson’s disease led to improvement of the rodent’s locomotive impairment.
“Our next step would be to continue using rodent or other suitable models to compare the outcomes of activating the FZD5 receptor and inhibiting GSK3,” said Yang. “These experiments will confirm which method is more effective in improving symptoms of Parkinson’s disease ahead of clinical trials.”
Funding: This research was supported by the University of Toronto Medicine by Design program, which receives funding from the Canada First Research Excellence Fund, and the Canadian Institutes of Health Research.
About this neurogenesis and Parkinson’s disease research news
Author: Anika Hazra
Source: University of Toronto
Contact: Anika Hazra – University of Toronto
Image: The image is credited to Neuroscience News
“Exploiting spatiotemporal regulation of FZD5 during neural patterning for efficient ventral midbrain specification” by Stephane Angers et al.
Friday, October 20, 2023
Effect of alcohol on Brain-Derived Neurotrophic Factor (BDNF) blood levels: a systematic review and meta-analysis
So maybe a change in my alcohol consumption or I just increase my BDNF levels other ways which your competent doctor should know all about.
But just in case s/he doesn't, my writeups on it:
BDNF (167 posts to April 2011)
BDNF also induces hippocampal long-term potentiation, which is important for memory formation [8]. Weinstein et al. found that higher peripheral BDNF levels protect the older adults against AD. By having BDNF levels higher by one standard deviation, the risk for AD or dementia was lowered by 33%
Effect of alcohol on Brain-Derived Neurotrophic Factor (BDNF) blood levels: a systematic review and meta-analysis
- Arman Shafiee,
- Kyana Jafarabady,
- Mohammad Ali Rafiei,
- Maryam Beiky,
- Niloofar Seighali,
- Golshid Golpayegani,
- Mehrsa Jalali,
- Faeze Soltani Abhari,
- Razman Arabzadeh Bahri,
- Omid Safari,
- Mahmood Bakhtiyari &
- Amirhesam Alirezaei
Scientific Reports volume 13, Article number: 17554 (2023) Cite this article
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125 Accesses
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1 Altmetric
Abstract
Brain-Derived Neurotrophic Factor (BDNF) is a vital protein involved in neuronal development, survival, and plasticity. Alcohol consumption has been implicated in various neurocognitive deficits and neurodegenerative disorders. However, the impact of alcohol on BDNF blood levels remains unclear. This systematic review and meta-analysis aimed to investigate the effect of alcohol consumption on BDNF blood levels. A comprehensive search of electronic databases was conducted to identify relevant studies. Eligible studies were selected based on predefined inclusion criteria. Data extraction was performed, and methodological quality was assessed using appropriate tools. A meta-analysis was conducted to estimate the overall effect size of alcohol consumption on BDNF levels. A total of 25 studies met the inclusion criteria and were included in the final analysis. Alcohol use and BDNF blood levels were significantly correlated, according to the meta-analysis (p = 0.008). Overall, it was discovered that drinking alcohol significantly decreased BDNF levels (SMD: − 0.39; 95% CI: − 0.68 to − 0.10; I2: 93%). There was a non-significant trend suggesting that alcohol withdrawal might increase BDNF levels, with an SMD of 0.26 (95% CI: − 0.09 to 0.62; I2: 86%; p = 0.14). Subgroup analysis based on the source of BDNF demonstrated significant differences between the subgroups (p = 0.0008). No significant publication bias was observed. This study showed that alcohol consumption is associated with a significant decrease in BDNF blood levels. The findings suggest a negative impact of alcohol on BDNF levels regardless of alcohol dosage. Further studies are needed to strengthen the evidence and elucidate the underlying mechanisms.
Introduction
Brain-Derived Neurotrophic Factor (BDNF) is a crucial protein that plays a vital role in the development, survival, and plasticity of neurons in the central nervous system1. It is involved in various neurobiological processes, including neuronal growth, differentiation, and synaptic plasticity2. BDNF is widely expressed in the brain, and its dysregulation has been implicated in the pathophysiology of numerous neurological and psychiatric disorders, such as depression, Alzheimer's disease, and substance use disorders2,3.
Alcohol consumption is a prevalent and culturally accepted practice in numerous societies4. It has been extensively studied for its detrimental effects on various organ systems, including the brain5. Chronic and excessive alcohol consumption is associated with a range of neurocognitive deficits, neurodegeneration, and increased vulnerability to psychiatric disorders6.Recent research has focused on elucidating the molecular mechanisms underlying alcohol's impact on brain function, with an increasing interest in its effects on BDNF7.
The association between alcohol consumption and BDNF levels has gained substantial attention due to its potential implications for understanding the neurobiological effects of alcohol on brain health8. Preclinical studies have demonstrated that alcohol exposure can modulate BDNF expression, leading to alterations in neuronal plasticity and impairments in cognitive functions8,9. Additionally, clinical studies have provided evidence of BDNF dysregulation in individuals with alcohol use disorders, further highlighting the importance of investigating the relationship between alcohol and BDNF levels10.
However, the existing literature on the effect of alcohol on BDNF blood levels is characterized by inconsistent findings, which may be attributed to variations in study design, participant characteristics, alcohol consumption patterns, and BDNF measurement methods. Therefore, this study aims to synthesize the current literature on the effect of alcohol consumption on BDNF blood levels through a rigorous and comprehensive analysis.
More at link.
Wednesday, May 26, 2021
MicroRNA-132 regulates neurogenesis in the hippocampus
Now we just need human testing and delivering it to the brain.
Maybe one of these:
MicroRNA-132, Delivered by Mesenchymal Stem Cell-Derived Exosomes, Promote Angiogenesis in Myocardial Infarction
Sustained delivery of proangiogenic microRNA-132 by nanoparticle transfection improves endothelial cell transplantation
The latest here:
MicroRNA-132 regulates neurogenesis in the hippocampus
Source: KNAW
Alzheimer’s disease is the main cause of dementia and current therapeutic strategies cannot prevent, slow down or cure the pathology. The disease is characterized by memory loss, caused by the degeneration and death of neuronal cells in several regions of the brain, including the hippocampus, which is where memories are initially formed.
Researchers from the Netherlands Institute for Neuroscience (NIN) have identified a small molecule that can be used to rejuvenate the brain and counteract the memory loss.
New cells in old brains
The presence of adult-born cells in the hippocampus of old people was recently demonstrated in scientific studies. It suggests that, generally speaking, the so-called process of adult neurogenesis is sustained throughout adulthood.
Adult neurogenesis is linked to several aspects of cognition and memory in both animal models and humans, and it was reported to sharply decrease in the brains of patients with Alzheimer’s disease.
Researchers also found that higher levels of adult neurogenesis in these patients seem to correlate with better cognitive performance before death.
“This could suggest that the adult-born neurons in our brain may contribute to a sort of cognitive reserve that could later on provide higher resilience to memory loss”, says Evgenia Salta, group leader at the NIN.
Therefore, researchers from the NIN investigated if giving a boost to adult neurogenesis could help prevent or improve dementia in Alzheimer’s disease.
A small molecule with big potential
Salta said, “Seven years ago, while studying a small RNA molecule that is expressed in our brain, called microRNA-132, we came across a rather unexpected observation. This molecule, which we had previously found to be decreased in the brain of Alzheimer’s patients, seemed to regulate homeostasis of neural stem cells in the central nervous system”.
Back then, Alzheimer’s was thought to be a disease affecting only mature neuronal cells, so at first glance this finding did not seem to explain a possible role of microRNA-132 in the progression of Alzheimer’s.
In this study, the researchers set out to address whether microRNA-132 can regulate adult hippocampal neurogenesis in healthy and Alzheimer’s brains. Using distinct Alzheimer’s mouse models, cultured human neural stem cells and post-mortem human brain tissue, they discovered that this RNA molecule is required for the neurogenic process in the adult hippocampus.
“Decreasing the levels of microRNA-132 in the adult mouse brain or in human neural stem cells in a dish impairs the generation of new neurons. However, restoring the levels of microRNA-132 in Alzheimer’s mice rescues neurogenic deficits and counteracts memory impairment related to adult neurogenesis”, Sarah Snoeck, technician in the group of Salta, explains.
These results provide a proof-of-concept regarding the putative therapeutic potential of bringing about adult neurogenesis in Alzheimer’s. Salta: “Our next goal is to systematically assess the efficacy and safety of targeting microRNA-132 as a therapeutic strategy in Alzheimer’s disease”.
Thursday, April 9, 2020
Intermittent fasting increases adult hippocampal neurogenesis
Now you need your doctors and hospital to initiate human research in this and specify how these newly created neurons will migrate to needed areas.
Maybe these might help:
Intermittent fasting increases adult hippocampal neurogenesis
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Associated Data
Abstract
Introduction
Methods
Results
Conclusions
Abstract

1. INTRODUCTION
Saturday, December 21, 2019
Early Stroke Induces Long-Term Impairment of Adult Neurogenesis Accompanied by Hippocampal-Mediated Cognitive Decline
There might be something here, but I don't know.
Early Stroke Induces Long-Term Impairment of Adult Neurogenesis Accompanied by Hippocampal-Mediated Cognitive Decline
Carolin Kathner-Schaffert 1, Lina Karapetow 1, Madlen Günther 1, Max Rudolph 1, Mahmoud Dahab 1, Eileen Baum 1, Thomas Lehmann 2, Otto W. Witte 1, Christoph Redecker 1, Christian W. Schmeer 1 and Silke Keiner 1,* 1 Hans-Berger Department of Neurology, Jena University Hospital, Am Klinikum 1, 07747 Jena, Germany; Carolin.Kathner-Schaffert@med.uni-jena.de (C.K.-S.); Lina.Karapetow@med.uni-jena.de (L.K.); Madlen.Guenther@med.uni-jena.de (M.G.); Max.Rudolph@uni-jena.de (M.R.); Mahmoud.Mohamed@med.uni-jena.de (M.D.); Eileen.Baum@noldus.com (E.B.); Otto.Witte@med.uni-jena.de (O.W.W.); Christoph.Redecker@klinikum-lippe.de (C.R.); Christian.Schmeer@med.uni-jena.de (C.W.S.) 2 Institute of Medical Statistics and Computer Science, University Hospital Jena, Friedrich Schiller University Jena, 07743 Jena, Germany; Thomas.Lehmann@med.uni-jena.de * Correspondence: silke.keiner@med.uni-jena.de; Tel.: +49-364-1932-5914Received: 14 October 2019; Accepted: 12 December 2019; Published: 17 December 2019
Abstract:
Stroke increases neurogenesis in the adult dentate gyrus in the short term, however, long-term effects at the cellular and functional level are poorly understood. Here we evaluated the impact of an early stroke lesion on neurogenesis and cognitive function of the aging brain. We hypothesized that a stroke disturbs dentate neurogenesis during aging correlate with impaired flexible learning. To address this issue a stroke was induced in 3-month-old C57Bl/6 mice by a middle cerebral artery occlusion (MCAO). To verify long-term changes of adult neurogenesis the thymidine analogue BrdU (5-Bromo-20-deoxyuridine) was administrated at different time points during aging. One and half months after BrdU injections learning and memory performance were assessed with a modified version of the Morris water maze (MWM) that includes the re-learning paradigm, as well as hippocampus-dependent and -independent search strategies. After MWM performance mice were transcardially perfused. To further evaluate in detail the stroke-mediated changes on stem- and progenitor cells as well as endogenous proliferation nestin-green-fluorescent protein (GFP) mice were used. Adult nestin-GFP mice received a retroviral vector injection in the hippocampus to evaluate changes in the neuronal morphology. At an age of 20 month the nestin-GFP mice were transcardially perfused after MWM performance and BrdU application 1.5 months later. The early stroke lesion significantly decreased neurogenesis in7.5-and 9-month-old animals and also endogenous proliferation in the latter group. Furthermore, immature double cortin (DCX)-positive neurons were reduced in 20-month-old nestin-GFP mice after lesion. All MCAO groups showed an impaired performance in the MWM and mostly relied on hippocampal independent search strategies. These findings indicate that an early ischemic insult leads to a dramatical decline of neurogenesis during aging that correlates with a premature development of hippocampal dependent deficits. Our study supports the notion that an early stroke might lead to long-term cognitive deficits as observed in human patients after lesion.
Sunday, June 16, 2019
Marijuana Chokes Alzheimer's-Related Brain Regions
I wouldn't trust anything here. Due to the use of SPECT scans by Dr. Amen they have a reputation as only being used to deceive. Do you really think neuropsychiatric patients would have normal brains? The selection of patients for this research shows its bias from the start.
My 13 reasons for marijuana use post-stroke.
Don't follow me, I'm not medically trained and I don't have a Dr. in front of my name.
Marijuana Chokes Alzheimer's-Related Brain Regions
In a big study of 26,000 people, the hippocampus "choked" on marijuana. (The hippocampus is the brain's memory and learning center.) Marijuana lowered blood flow to levels unseen in any other group. Find out why this strongly suggests higher vulnerability to Alzheimer’s.
As the U.S. races to legalize marijuana for medicinal and recreational use, a large scale brain imaging study gives reason for caution. Published in the Journal of Alzheimer’s Disease, researchers using single photon emission computed tomography (SPECT), a sophisticated imaging study that evaluates blood flow and activity patterns, demonstrated abnormally low blood flow in virtually every area of the brain, in nearly 1,000 marijuana users compared to healthy controls.
Marijuana, Alzheimer's & the Hippocampus
The marijuana users' low blood flow patterns included areas known to be affected by Alzheimer’s pathology such as the hippocampus.Continued below image...
IMAGE LEGEND: Example of a volume rendered brain SPECT image (top down view) of a healthy control compared to an 18-year old daily user of marijuana. While the control subject has symmetric activity, the marijuana user shows overall decreased perfusion.
All data were obtained for analysis from a large multi-site database, involving 26,268 patients who came for evaluation of complex, treatment resistant issues to one of nine outpatient neuropsychiatric clinics across the United States (Newport Beach, Costa Mesa, Fairfield, and Brisbane, CA, Tacoma and Bellevue, WA, Reston, VA, Atlanta, GA and New York, NY) between 1995-2015. Of these, 982 current or former marijuana users had brain SPECT at rest and during a mental concentration task compared to almost 100 healthy controls. Predictive analytics with discriminant analysis was done to determine if brain SPECT regions can distinguish marijuana user brains from controls brain.
Low Blood Flow
Low blood flow in the hippocampus in marijuana users reliably distinguished marijuana users from controls. The right hippocampus during a concentration task was the single most predictive region in distinguishing marijuana users from their normal counterparts. Marijuana use is thought to interfere with memory formation by inhibiting activity in this part of the brain.According to one of the co-authors on the study Elisabeth Jorandby, M.D., “As a physician who routinely sees marijuana users, what struck me was not only the global reduction in blood flow in the marijuana users brains, but that the hippocampus was the most affected region due to its role in memory and Alzheimer’s disease."
May Be Harbingers of Brain Damage
She continued, "Our research has proven that marijuana users have lower cerebral blood flow than non-users. Second, the most predictive region separating these two groups is low blood flow in the hippocampus on concentration brain SPECT imaging. This work suggests that marijuana use has damaging influences in the brain – particularly regions important in memory and learning and known to be affected by Alzheimer’s.”Dr. George Perry, Editor in Chief of the Journal of Alzheimer’s Disease said, “Open use of marijuana, through legalization, will reveal the wide range of marijuana’s benefits and threats to human health. This study indicates troubling effects on the hippocampus that may be the harbingers of brain damage.”
- Amen DG, Darmal B, Raji CA, Bao W, Jorandby L, Meysami S, Raghavendra CS (2017) Discriminative Properties of Hippocampal Hypoperfusion in Marijuana Users Compared to Healthy Controls: Implications for Marijuana Administration in Alzheimer’s Dementia. J Alzheimers Dis, doi: 10.3233/JAD-160833.
- Figure legend: Example of a volume rendered brain SPECT image (top down view) of a healthy control compared to an 18-year old daily user of marijuana. While the control subject has symmetric activity, the marijuana user shows overall decreased perfusion.
Sunday, June 2, 2019
Sexual Experience Promotes Adult Neurogenesis in the Hippocampus Despite an Initial Elevation in Stress Hormones
If I'm reading this correctly and can extrapolate to humans for those who get this post stroke anxiety(20% chance) your doctor should be ensuring you have sex at least 14 days in a row. Which way will your doctor be incompetent? NOT knowing, Or NOT doing? Some bias here, they did not test female rats.
Sexual Experience Promotes Adult Neurogenesis in the Hippocampus Despite an Initial Elevation in Stress Hormones
- Benedetta Leuner,
- Erica R. Glasper,
- Elizabeth Gould
- Published: July 14, 2010
- https://doi.org/10.1371/journal.pone.0011597
Abstract
Aversive stressful experiences are typically associated with increased anxiety and a predisposition to develop mood disorders. Negative stress also suppresses adult neurogenesis and restricts dendritic architecture in the hippocampus, a brain region associated with anxiety regulation. The effects of aversive stress on hippocampal structure and function have been linked to stress-induced elevations in glucocorticoids. Normalizing corticosterone levels prevents some of the deleterious consequences of stress, including increased anxiety and suppressed structural plasticity in the hippocampus. Here we examined whether a rewarding stressor, namely sexual experience, also adversely affects hippocampal structure and function in adult rats. Adult male rats were exposed to a sexually-receptive female once (acute) or once daily for 14 consecutive days (chronic) and levels of circulating glucocorticoids were measured. Separate cohorts of sexually experienced rats were injected with the thymidine analog bromodeoxyuridine in order to measure cell proliferation and neurogenesis in the hippocampus. In addition, brains were processed using Golgi impregnation to assess the effects of sexual experience on dendritic spines and dendritic complexity in the hippocampus. Finally, to evaluate whether sexual experience alters hippocampal function, rats were tested on two tests of anxiety-like behavior: novelty suppressed feeding and the elevated plus maze. We found that acute sexual experience increased circulating corticosterone levels and the number of new neurons in the hippocampus. Chronic sexual experience no longer produced an increase in corticosterone levels but continued to promote adult neurogenesis and stimulate the growth of dendritic spines and dendritic architecture. Chronic sexual experience also reduced anxiety-like behavior. These findings suggest that a rewarding experience not only buffers against the deleterious actions of early elevated glucocorticoids but actually promotes neuronal growth and reduces anxiety.Figures
Editor: Melissa Coleman, Claremont Colleges, United States of America
Received: March 30, 2010; Accepted: June 17, 2010; Published: July 14, 2010
Copyright: © 2010 Leuner et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.
Funding: The work was supported by a Young Investigator Award from the National Alliance for Research on Schizophrenia and Depression (B.L.), grants from the National Institute of Mental Health (MH084148 to B.L. and MH54970 to E.G.) and a Ruth L. Kirschstein postdoctoral NRSA fellowship from the National Institute on Aging (E.R.G.). The funders had no role in study design, data collection and analysis, decision to publish, or preparation of the manuscript.
Friday, April 6, 2018
Older adults can still grow new brain cells, study finds
https://www.cbsnews.com/news/older-adults-can-grow-new-brain-cells-study-finds/