Changing stroke rehab and research worldwide now.Time is Brain! trillions and trillions of neurons that DIE each day because there are NO effective hyperacute therapies besides tPA(only 12% effective). I have 523 posts on hyperacute therapy, enough for researchers to spend decades proving them out. These are my personal ideas and blog on stroke rehabilitation and stroke research. Do not attempt any of these without checking with your medical provider. Unless you join me in agitating, when you need these therapies they won't be there.

What this blog is for:

My blog is not to help survivors recover, it is to have the 10 million yearly stroke survivors light fires underneath their doctors, stroke hospitals and stroke researchers to get stroke solved. 100% recovery. The stroke medical world is completely failing at that goal, they don't even have it as a goal. Shortly after getting out of the hospital and getting NO information on the process or protocols of stroke rehabilitation and recovery I started searching on the internet and found that no other survivor received useful information. This is an attempt to cover all stroke rehabilitation information that should be readily available to survivors so they can talk with informed knowledge to their medical staff. It lays out what needs to be done to get stroke survivors closer to 100% recovery. It's quite disgusting that this information is not available from every stroke association and doctors group.

Wednesday, January 22, 2025

Human Hippocampal Neurogenesis Persists throughout Aging

Has your competent? doctor and hospital powered the research that figured out how to migrate new neurons from the hippocampus to where they are needed? We've known of this need for years. The least your doctor could do is ensure this research gets to human testing.

hippocampal neurogenesis (3 posts to December 2020)

hippocampus (77 posts to October 2011)

neurogenesis (597 posts to September 2010)

The latest here: 

Human Hippocampal Neurogenesis Persists throughout Aging

Cover Image - Cell Stem Cell, Volume 22, Issue 4

Highlights

Pools of quiescent stem cells are smaller in aged human hippocampal dentate gyri
Proliferating progenitor and immature neuron pools are stable with aging
Angiogenesis and neuroplasticity decline in older humans
Granule neurons, glia, and dentate gryus volume are unchanged with aging

Summary

Adult hippocampal neurogenesis declines in aging rodents and primates. Aging humans are thought to exhibit waning neurogenesis and exercise-induced angiogenesis, with a resulting volumetric decrease in the neurogenic hippocampal dentate gyrus (DG) region, although concurrent changes in these parameters are not well studied. Here we assessed whole autopsy hippocampi from healthy human individuals ranging from 14 to 79 years of age. We found similar numbers of intermediate neural progenitors and thousands of immature neurons in the DG, comparable numbers of glia and mature granule neurons, and equivalent DG volume across ages. Nevertheless, older individuals have less angiogenesis and neuroplasticity and a smaller quiescent progenitor pool in anterior-mid DG, with no changes in posterior DG. Thus, healthy older subjects without cognitive impairment, neuropsychiatric disease, or treatment display preserved neurogenesis. It is possible that ongoing hippocampal neurogenesis sustains human-specific cognitive function throughout life and that declines may be linked to compromised cognitive-emotional resilience.

Graphical Abstract

Graphical abstract undfig1

Keywords

  1. dentate gyrus
  2. Sox2
  3. nestin
  4. Ki-67
  5. PSA-NCAM
  6. NeuN
  7. doublecortin
  8. granule cells
  9. neural progenitor
  10. volume

Introduction

Healthy aging is crucial in a growing older population (). The ability to separate similar memory patterns () and recover from stress () may depend on adult hippocampal neurogenesis (AHN), which is reported to decline with aging in nonhuman primates () and mice (). New neurons are generated in the dentate gyrus (DG) of the adult human hippocampus, even after middle age (), but the extent to which neurogenesis occurs in humans is highly debated and quantitative studies are scarce.
Phylogenetic differences between humans and rodents mandate assessment of the different stages of neuronal maturation in the human DG. For example, striatal neurogenesis is found only in humans (), while olfactory bulb neurogenesis is absent in humans () but present in other mammals. Previous analyses of human AHN did not address the effects of aging, although studies have examined AHN in older populations (). The density of doublecortin-positive (DCX+) cells were reported to decline from birth into the tenth decade of life () in parallel with 14C-determined neuron turnover (); however, medication and drug use, which affect AHN (), were not addressed (). Using histological techniques that could not distinguish mature and immature neurons, several groups estimated that DG neurons did not decline in aging humans ().
In vivo brain imaging studies reported conflicting findings regarding age-related changes in specific hippocampal regions. While some studies observed age-related declines in anterior hippocampal volume (), others found no volume change (), or altered hippocampal shape rather than volume (). Efforts to evaluate AHN in vivo face limitations due to inadequate spatial resolution and the inability to accurately differentiate hippocampal sub-regions ().
AHN and angiogenesis are co-regulated (). Exercise enhances cerebral blood volume, which results in more AHN in mice and better cognitive performance in humans (), but it may have a reduced impact in older people (). Thus, we quantified AHN, angiogenesis, and DG volume and their relationship in people of different ages, hypothesizing that they would concurrently decrease with aging and correlate with each other.
Given the different functions of the rostral and caudal DG (), we assessed the anterior, mid, and posterior hippocampus postmortem from 28 women and men 14 to 79 years of age. In each region, we characterized and quantified angiogenesis, volume, and cells at different maturational stages in the DG neurogenic niche, using unbiased stereological methods (). To avoid confounders, subjects studied had no neuropsychiatric disease or treatment.
Healthy elderly people have the potential to remain cognitively and emotionally more intact than commonly believed, due to the persistence of AHN into the eighth decade of life. However, reduced cognitive-emotional resilience may be caused by a variety of factors such as a smaller quiescent neural progenitor pool, diminished angiogenesis, or decreasing neuroplasticity in the anterior DG.

Results

The generation of new neurons in the DG neurogenic niche starts from quiescent radial-glia-like type I neural progenitor cells (QNPs) expressing glial fibrillary acid protein (GFAP), sex determining region Y-box 2 (Sox2), brain lipid-binding protein (BLBP), and nestin (). QNPs undergo asymmetric divisions and generate amplifying, or type II, intermediate neural progenitors (INPs) expressing Ki-67 and nestin (). As type II INPs differentiate into neuroblasts, or type III INPs, they lose the expression of Sox2 and GFAP while gaining expression of DCX and polysialylated neural cell adhesion molecule (PSA-NCAM), which is also expressed by immature and mature granule neurons (GNs) (). GNs are the final product of the differentiation cascade and express neuronal nuclear marker (NeuN), Prox-1, calbindin, and βIII-tubulin (). In anterior, mid, and posterior DG, we characterized and quantified the following: QNPs expressing GFAP, Sox2, and nestin; type I and II INPs expressing Ki-67 and nestin; neuroblasts, or type III INPs, and immature GNs expressing DCX and PSA-NCAM; and finally, mature GNs expressing NeuN. The anterior DG was defined as the portion from the most rostral appearance of the DG to the start of the lateral geniculate (visible in coronal brain sections); the mid DG spanned the lateral geniculate; and the posterior DG went from the end of the lateral geniculate to the caudal end of the DG.

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