Abstract
A reduction of neurosteroids in the brain may initiate sporadic Alzheimers disease (AD) which comprises > 99% of all AD cases. AD research is currently focused on aberrant amyloid precursor protein (APP) processing and the hyper-phosphorylation of tau protein. This is based on early-onset genetic and pathological observations clearly showing that these markers are involved in the progression of the disease. However, there is still ongoing debate as to the key pathological events in the sporadic form of AD where the Aβ and tau genes are not usually mutated. The vulnerability of the transentorhinal cortex, which displays the first architectural signs of AD, may be related to its role as the entry point for an enormous amount of excitatory information, the majority from the neocortex, which passes through the hippocampal formation. Neurosteroids provide a layer of protection from excessive excitation, and their age-related decrease may expose the vulnerability required to allow neuronal death by excitotoxicity and thereby initiate the disease.
Keywords: Sporadic (AD), Neurosteroids, hyper-phosphorylation, tau protein, transentorhinal cortex, neocortex, excitotoxicity
Current Alzheimer Research
Title: Neurosteroids and Sporadic Alzheimers Disease
Volume: 5 Issue: 4
Author(s): Guy Barry and Ian L. Ross
Affiliation:
Keywords: Sporadic (AD), Neurosteroids, hyper-phosphorylation, tau protein, transentorhinal cortex, neocortex, excitotoxicity
Abstract: A reduction of neurosteroids in the brain may initiate sporadic Alzheimers disease (AD) which comprises > 99% of all AD cases. AD research is currently focused on aberrant amyloid precursor protein (APP) processing and the hyper-phosphorylation of tau protein. This is based on early-onset genetic and pathological observations clearly showing that these markers are involved in the progression of the disease. However, there is still ongoing debate as to the key pathological events in the sporadic form of AD where the Aβ and tau genes are not usually mutated. The vulnerability of the transentorhinal cortex, which displays the first architectural signs of AD, may be related to its role as the entry point for an enormous amount of excitatory information, the majority from the neocortex, which passes through the hippocampal formation. Neurosteroids provide a layer of protection from excessive excitation, and their age-related decrease may expose the vulnerability required to allow neuronal death by excitotoxicity and thereby initiate the disease.
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Cite this article as:
Barry Guy and Ross L. Ian, Neurosteroids and Sporadic Alzheimers Disease, Current Alzheimer Research 2008; 5 (4) . https://dx.doi.org/10.2174/156720508785132325
DOI https://dx.doi.org/10.2174/156720508785132325 |
Print ISSN 1567-2050 |
Publisher Name Bentham Science Publisher |
Online ISSN 1875-5828 |
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