Reconsidering Alzheimer’s Pathology And Hippocampal Neurogenesis.

1099 words - 5 pages

Most investigations using transgenic animal models of Alzheimer’s disease (AD) have reported a decrease in hippocampal neurogenesis. Currently, is considered that an impairment in neurogenesis can be an important factor during the onset and progression of AD. Most authors consider hippocampal neurogenesis necessary to maintain hippocampal cognitive abilities, therefore, a damage in the proliferative system has to be functionally detrimental (See references in Mu and Gage, 2011). Most animal models with the familial type mutations that cause AD show that when toxic amyloid beta peptides (Aβ42) are present, hippocampal neurogenesis decreases. In addition, we know that knocking out of presenilin-1 in the hippocampus impairs proliferation. The general agreement is that all mutations related with AD should be damaging for adult neurogenesis with the consequent cognitive impairment. Considering this, it is notorious that for the surprise of the authors, Yetman and Jankowsky (2013) showed no impact on neurogenesis caused by a strong Human amyloid precursor protein (hAPP) overexpression. This happens when hAPP expression excludes the proliferative area of the dentate gyrus.
In front of a large amount of data obtained from animal models, how neurogenesis responds to AD in humans remains understudied. Still, the available evidence show either no alteration on neurogenesis during AD or a significant increase on proliferation and survival of new neurons (Jin et al., 2004, Perry et al., 2012). In 2004, Jin and colleagues showed that AD increases neurogenesis markers, not only during the onset, but also during the middle and advanced stages of the disease. In addition, a more detailed studied presented in 2012 by Perry and colleagues showed cell counts from six stages of the disease. In this work is very clear that both the cell progenitor’s (Nestin+ cells) and immature new neurons (Doublecortin+ and PSA-NCAM+ cells) populations increases. The authors contrasted hippocampal and ventricular neurogenesis; results are similar in the two human brain neurogenic niches, suggesting a similar regulation of all progenitor cells during AD. In the light of these results, some authors suggest that neurogenesis may substitute cells and repair damage after AD. This repair hypothesis would explain the odd case of neurogenesis increase during AD in humans. The main problem with this view is that the dentate gyrus does not present cell loss during AD (West et al., 1994); therefore, the neuronal substitution here would result in a misplaced waste of resources.
In the paper of Yetman and Jankowsky, they generate a familial AD model in which the mature glutamatergic cells would overexpress a mutant hAPP, expressed in cells that release Aβ42. The pattern of Aβ42 deposition is normal and amyloid plaques cover the hippocampus and its dentate gyrus molecular layer. However, progenitors and immature neurons do not produce hAPP and no plaques are found around them. The nonspecific...

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