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
Keywords
Introduction
Healthy aging is crucial in a growing older population (United States Census Bureau, 2017). The ability to separate similar memory patterns (Sahay et al., 2011) and recover from stress (Schloesser et al., 2010) may depend on adult hippocampal neurogenesis (AHN), which is reported to decline with aging in nonhuman primates (Leuner et al., 2007) and mice (Ben Abdallah et al., 2007). New neurons are generated in the dentate gyrus (DG) of the adult human hippocampus, even after middle age (Eriksson et al., 1998), 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 (Bergmann et al., 2015), while olfactory bulb neurogenesis is absent in humans (Bergmann et al., 2012)
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 (Eriksson et al., 1998). The density of doublecortin-positive (DCX+) cells were reported to decline from birth into the tenth decade of life (Knoth et al., 2010) in parallel with 14C-determined neuron turnover (Bergmann et al., 2015); however, medication and drug use, which affect AHN (Boldrini et al., 2014), were not addressed (Knoth et al., 2010; Sorrells et al., 2018; Spalding et al., 2013).
Using histological techniques that could not distinguish mature and
immature neurons, several groups estimated that DG neurons did not
decline in aging humans (Harding et al., 1998; Simić et al., 1997; West et al., 1994).
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 (Malykhin et al., 2008), others found no volume change (Head et al., 2005), or altered hippocampal shape rather than volume (Yang et al., 2013). Efforts to evaluate AHN in vivo face limitations due to inadequate spatial resolution and the inability to accurately differentiate hippocampal sub-regions (Ho et al., 2013; Manganas et al., 2007; Ramm et al., 2009).
AHN and angiogenesis are co-regulated (Boldrini et al., 2012; Heine et al., 2005; Thored et al., 2007; Warner-Schmidt and Duman, 2007). Exercise enhances cerebral blood volume, which results in more AHN in mice and better cognitive performance in humans (Pereira et al., 2007), but it may have a reduced impact in older people (Maass et al., 2015).
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 (Wu and Hen, 2014), 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 (West, 1993). 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 (Encinas et al., 2011).
QNPs undergo asymmetric divisions and generate amplifying, or type II,
intermediate neural progenitors (INPs) expressing Ki-67 and nestin (Encinas et al., 2011).
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) (Encinas et al., 2011).
GNs are the final product of the differentiation cascade and express
neuronal nuclear marker (NeuN), Prox-1, calbindin, and βIII-tubulin (Encinas et al., 2011).
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.
More at link.
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