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. Did your doctor somehow miss the recovery protocol that Pedro Bach-y-Rita used to recover fully back in 1958 with only a partial brain?

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.

Showing posts with label hippocampus. Show all posts
Showing posts with label hippocampus. Show all posts

Wednesday, July 8, 2026

Psilocybin reduces fear memory and restores neuroplasticity in the hippocampus and medial prefrontal cortex

 

Of course your competent? doctor ignored all the previous positive research on psilocybin for stroke! Over a decade of incompetence!

psilocybin (56 posts to May 2014)


Psilocybin reduces fear memory and restores neuroplasticity in the hippocampus and medial prefrontal cortex


Abstract

Background:

 Posttraumatic stress disorder (PTSD) and major depressive disorder are often comorbid in humans. Psilocybin reportedly has beneficial therapeutic effects on depression, possibly by promoting neuroplasticity. PTSD is associated with the dysregulation of neuroplasticity in the hippocampus and medial prefrontal cortex (mPFC). We hypothesized that psilocybin might reduce fear memory by promoting neuroplasticity in the hippocampus and mPFC.
 We investigated the effects of psilocybin on fear memory and explored its underlying mechanisms. We generated a mouse model of PTSD via auditory-cued fear conditioning and treated the mice with either vehicle or psilocybin (2.5 mg/kg, intraperitoneal) on day 0. Fear memory was assessed by the percentage of freezing time in response to conditioned stimuli. Fear memory tests were conducted on days 1, 6, and 7, after which the mice were sacrificed. To investigate the role of neuroplasticity in mediating the effects of psilocybin on fear memory, we assessed structural neuroplasticity and neuroplasticity-associated marker protein levels in the hippocampus and mPFC 7 days after a single dose of psilocybin.

Results:

Psilocybin reduced the cue-induced fear response on days 1, 6, and 7. Psilocybin ameliorated the fear conditioning-induced decreases in neuroplasticity in the hippocampus and mPFC. Through Golgi-Cox staining, Western blotting, and immunofluorescence staining, we found that psilocybin increased dendritic branches and spine density, upregulated GluR1 and synapsin-1, enhanced brain-derived neurotrophic factor and mammalian target of rapamycin signaling, and promoted neurogenesis.

Conclusions:

A single dose of psilocybin reduces both the rapid and sustained fear memory in mice, at least in part by restoring neuroplasticity in the hippocampus and mPFC. These findings indicate that psilocybin has significant potential for use in the treatment of PTSD and other mental disorders characterized by fear memory.

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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:

  1. 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.
  2. 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.
  3. 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.

This shows neurons.
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. Credit: Neuroscience News

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

Original Research: Open access.
“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

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

ummary: MicroRNA-132 regulates neurogenesis in the hippocampus, according to both mouse and human tissue studies. Restoring levels of microRNA-132 in mouse models of Alzheimer’s disease reduces neurogenetic deficits and restores cognitive abilities, researchers say.

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

Associated Data

Data Availability Statement

Abstract

Introduction

Intermittent fasting (IF) has been suggested to have neuroprotective effects through the activation of multiple signaling pathways. Rodents fasted intermittently exhibit enhanced hippocampal neurogenesis and long‐term potentiation (LTP) at hippocampal synapses compared with sedentary animals fed an ad libitum (AL) diet. However, the underlying mechanisms have not been studied. In this study, we evaluated the mechanistic gap in understanding IF‐induced neurogenesis.

Methods

We evaluated the impact of 3 months of IF (12, 16, and 24 hr of food deprivation on a daily basis) on hippocampal neurogenesis in C57BL/6NTac mice using immunoblot analysis.

Results

Three‐month IF significantly increased activation of the Notch signaling pathway (Notch 1, NICD1, and HES5), neurotrophic factor BDNF, and downstream cellular transcription factor, cAMP response element‐binding protein (p‐CREB). The expression of postsynaptic marker, PSD95, and neuronal stem cell marker, Nestin, was also increased in the hippocampus in response to 3‐month IF.

Conclusions

These findings suggest that IF may increase hippocampal neurogenesis involving the Notch 1 pathway.
Keywords: brain‐derived neurotrophic factor, hippocampus, intermittent fasting, neurogenesis, Notch

Abstract

Intermittent fasting (IF) is a dietary protocol where energy restriction is induced by alternate periods of ad libitum feeding and fasting. The present study has sought to investigate the relationship between IF and hippocampal neurogenesis. Our findings suggest that IF may increase hippocampal neurogenesis involving the Notch 1 pathway.
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Object name is BRB3-10-e01444-g005.jpg

1. INTRODUCTION

Dietary restriction (DR) is defined as a decrease in energy consumption without reducing nutritional value. This simple dietary intervention has been shown in a wide range of experimental animals to extend lifespan and decrease the incidence of several age‐related diseases. The definition of DR has been expanded from an alternative description of caloric restriction (CR) to also encompass a broader scope of interventions, including short‐term starvation, periodic fasting, fasting‐mimetic diets, and intermittent fasting (IF; Mattson & Arumugam, 2018). IF has been proven to be advantageous to various organ systems in the body and acts as a mild metabolic stressor. It has been postulated that IF is able to cause powerful changes in the metabolic pathways in the brain via an increase in stress resistance, and breakdown of ketogenic amino acids and fatty acids (Bruce‐Keller, Umberger, McFall, & Mattson, 1999; Kim et al., 2018). Experimental studies have also shown that IF is neuroprotective against acute brain injuries such as stroke, and neurodegenerative diseases (Arumugam et al., 2010; Halagappa et al., 2007; Manzanero et al., 2014). In addition, recent studies have also shown that IF can lead to an increase in neurogenesis levels in the hippocampus (Manzanero et al., 2014).
In the adult brain, the niches of neuronal stem cells (NSCs) are located specifically at the subventricular zone (SVZ) of the lateral ventricles, and in the subgranular zone (SGZ) of the hippocampus. The ability of NSCs to maintain cerebral neurogenesis is controlled by the tight regulation of balanced events commencing from stem cell maintenance, to stem cell division and proliferation, to its differentiation into mature neurons, and finally their survival and functional integration into the brain parenchyma (Lathia, Mattson, & Cheng, 2008; Lledo, Alonso, & Grubb, 2006). The process of adult neurogenesis is highly regulated and is adaptable to environmental, morphological, and physiological cues, whereby cerebral performance is suited to function at optimal levels for a given environment. Studies have demonstrated that the proliferation of neural stem cells can be modified through metabolic perturbations experienced during high temperatures (Matsuzaki et al., 2009), physical activity (Niwa et al., 2016), and a high‐fat diet (Kokoeva, Yin, & Flier, 2005). Experimental studies from our group have also shown that IF increases neurogenesis in the hippocampus as a form of neuroprotection following acute brain injury such as ischemic stroke. Moreover, we established that the number of BrdU‐labeled cells in the dentate gyrus of IF mice was elevated (Manzanero et al., 2014). To measure cell proliferation without the confound availability of an exogenous marker BrdU, we established increases in the number of Ki67‐labeled cells in the dentate gyrus of mice on the IF diet, indicating enhancement of cell proliferation in these mice (Manzanero et al., 2014). In addition to our findings, previous work similarly demonstrated that using the every other day (EOD) IF regimen also increased BrdU‐labeled cell number in the hippocampus (Lee, Duan, & Mattson, 2002).
However, the molecular process involved in IF‐induced neurogenesis is not well understood. The Notch signaling pathway that is intricately involved in the determination of cell fate during brain development and adult neurogenesis may be a possible molecular process involved in IF‐induced neurogenesis (Lathia et al., 2008). In this study, we investigated the expression levels of molecular and cellular components of the hippocampal region, focusing specifically on Notch activation and associated proteins that are known to promote hippocampal neurogenesis such as brain‐derived neurotrophic factor (BDNF) and cAMP response element‐binding protein (CREB).

More at link.

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.: +49-364-1932-5914
Received: 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

PREVENTION & THERAPY NEWS:
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.”


MORE INFORMATION:
SOURCE:

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
PLOS
x





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.


Friday, April 6, 2018

Older adults can still grow new brain cells, study finds

I hope the neurogenesis research finally determines that it does exist. I'm planning on using neurogenesis to fully recover. I see no hope for stem cells in my lifetime.
https://www.cbsnews.com/news/older-adults-can-grow-new-brain-cells-study-finds/
Contrary to popular thought, older adults' brains can churn out just as many new cells as younger brains do, a new study suggests.
Using autopsied brain tissue, researchers found that healthy older adults had the same capacity to create new cells in the brain's hippocampus region as young adults did.
The hippocampus is involved in regulating memory and emotions, and it typically shrinks in people with Alzheimer's disease, according to the Alzheimer's Association.
The new findings give a snapshot of the healthy aging brain -- and it's a "positive" one, the researchers said.
In general, old and young brains were capable of making the same number of new neurons from more primitive "progenitor" cells in the hippocampus.
"It's good news that these cells are there in older adults' brains," said lead researcher Dr. Maura Boldrini, an associate professor at Columbia University in New York City.
That's not to say that the brain of a healthy 79-year-old looks exactly like the brain of a healthy 29-year-old.
For example, the investigators found that older adults' brains had less "angiogenesis" -- or new blood vessel growth.
So it's not clear whether the new brain cells would have the same connections, or function the same as younger adult brain cells do, noted Dr. Ezriel Kornel. He is an assistant clinical professor of neurosurgery at Weill Cornell Medical College in New York City.
But Kornel, who was not involved in the study, said the findings offer a "hopeful" message.
"Even as we age," he said, "we still have the capability of producing new neurons."
More research is needed to understand what factors can help "stimulate" greater neuron production or better connectivity in older brains, Kornel added.
Lab research has found that in aging rodents and non-human primates, the hippocampus loses its ability to churn out new cells. But studies of the human brain have come to conflicting conclusions.
That's partly because researchers weren't always able to account for any brain diseases people might have had before death, Boldrini explained.
Her team examined autopsied brain tissue from 28 people between the ages of 14 and 79 who'd died suddenly, but had previously been healthy. None had been diagnosed with dementia, or any neurological or psychiatric disorder.
Overall, the study found, older and younger brains had similar numbers of "intermediate" progenitor cells and "immature" neurons -- signaling that older people had a similar capacity for generating new cells as young people.
There were differences, however. Besides having less angiogenesis, the older brains also had a smaller pool of progenitor cells in one area of the hippocampus.
It would be interesting, Kornel said, to see how those healthy older brains compare with those of older adults who did suffer from dementia.
Boldrini agreed, and said that's a next step. Other research, she noted, has found a decreased number of neurons in the hippocampus of people who died with Alzheimer's.
But it's not clear what causes that. "Does the brain produce fewer neurons? Or did the neurons die?" Boldrini said.
By comparing healthy older brains and dementia-affected brains, she said, researchers could gain a better understanding of why some people stay sharp well into old age, while others decline.
That might lead to new treatments for dementia, Boldrini said -- if research can uncover some of the molecular mechanisms that support neuron production and survival in older brains.
Plus, she added, it's important to figure out whether older adults who maintain a youthful-looking hippocampus did something "right" over their lifetime -- whether that's diet, regular exercise or meditation.

Thursday, February 8, 2018

Is silence golden? Effects of auditory stimuli and their absence on adult hippocampal neurogenesis

Four years and I bet your doctor and stroke hospital have done nothing to create a silence protocol. Are they that fucking incompetent? Yes they are. What are you going to do about that? 

Is silence golden? Effects of auditory stimuli and their absence on adult hippocampal neurogenesis


Brain Struct Funct. 2015; 220(2): 1221–1228.
Published online 2013 Dec 1. doi:  10.1007/s00429-013-0679-3

Abstract

We have previously hypothesized that the reason why physical activity increases precursor cell proliferation in adult neurogenesis is that movement serves as non-specific signal to evoke the alertness required to meet cognitive demands. Thereby a pool of immature neurons is generated that are potentially recruitable by subsequent cognitive stimuli. Along these lines, we here tested whether auditory stimuli might exert a similar non-specific effect on adult neurogenesis in mice. We used the standard noise level in the animal facility as baseline and compared this condition to white noise, pup calls, and silence. In addition, as patterned auditory stimulus without ethological relevance to mice we used piano music by Mozart (KV 448). All stimuli were transposed to the frequency range of C57BL/6 and hearing was objectified with acoustic evoked potentials. We found that except for white noise all stimuli, including silence, increased precursor cell proliferation (assessed 24 h after labeling with bromodeoxyuridine, BrdU). This could be explained by significant increases in BrdU-labeled Sox2-positive cells (type-1/2a). But after 7 days, only silence remained associated with increased numbers of BrdU-labeled cells. Compared to controls at this stage, exposure to silence had generated significantly increased numbers of BrdU/NeuN-labeled neurons. Our results indicate that the unnatural absence of auditory input as well as spectrotemporally rich albeit ethological irrelevant stimuli activate precursor cells—in the case of silence also leading to greater numbers of newborn immature neurons—whereas ambient and unstructured background auditory stimuli do not.