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On a New Paradigm of the Development of Neurodegenerative Diseases by the Example of Alzheimer’s Disease and Parkinson’s Disease

On a New Paradigm of the Development of Neurodegenerative Diseases by the Example of Alzheimer’s... The role of neuronal inflammation developing during the formation of amyloid plaques and Lewy bodies is investigated. The influence of various exogenous and endogenous factors on the development of neuroinflammation is established, but the role of various infectious agents in the development of this process is much less studied. Today, the existence of a universal trigger mechanism of the neurodegenerative process is obvious: a specific pathogen of a bacterial or viral nature (including long-term persistent in nervous tissue in a latent state), reactivating, penetrates into certain cerebral structures, where it is influenced by either Aβ or resident macrophages of the central nervous system, which, in turn, are activated and induce the release of proinflammatory cytokines, leading to the development of neuronal inflammation, autophagy and neurodegeneration. The reactivation of latent infection, such as herpes, in APOE4 carriers significantly increases the risk of development of Alzheimer’s disease. Class-II genes of the HLA locus (HLA II) may be related to the progression of neurodegenerative diseases. An increase in iron levels in the glia is induced by inflammation, which leads to neurodegeneration. Disruption of the homeostasis of redox-active metals, iron and copper, is an integral part of the pathogenesis of Alzheimer’s disease and Parkinson’s disease. The developing neuroinflammation leads to intensification of the processes of peroxidation, oxidation of metals and the development of ferroptosis. http://www.deepdyve.com/assets/images/DeepDyve-Logo-lg.png Advances in Gerontology Springer Journals

On a New Paradigm of the Development of Neurodegenerative Diseases by the Example of Alzheimer’s Disease and Parkinson’s Disease

Advances in Gerontology , Volume 12 (4) – Dec 1, 2022

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References (77)

Publisher
Springer Journals
Copyright
Copyright © Pleiades Publishing, Ltd. 2022. ISSN 2079-0570, Advances in Gerontology, 2022, Vol. 12, No. 4, pp. 386–395. © Pleiades Publishing, Ltd., 2022. Russian Text © The Author(s), 2022, published in Uspekhi Gerontologii, 2022, Vol. 35, No. 2, pp. 263–273.
ISSN
2079-0570
eISSN
2079-0589
DOI
10.1134/s2079057022040117
Publisher site
See Article on Publisher Site

Abstract

The role of neuronal inflammation developing during the formation of amyloid plaques and Lewy bodies is investigated. The influence of various exogenous and endogenous factors on the development of neuroinflammation is established, but the role of various infectious agents in the development of this process is much less studied. Today, the existence of a universal trigger mechanism of the neurodegenerative process is obvious: a specific pathogen of a bacterial or viral nature (including long-term persistent in nervous tissue in a latent state), reactivating, penetrates into certain cerebral structures, where it is influenced by either Aβ or resident macrophages of the central nervous system, which, in turn, are activated and induce the release of proinflammatory cytokines, leading to the development of neuronal inflammation, autophagy and neurodegeneration. The reactivation of latent infection, such as herpes, in APOE4 carriers significantly increases the risk of development of Alzheimer’s disease. Class-II genes of the HLA locus (HLA II) may be related to the progression of neurodegenerative diseases. An increase in iron levels in the glia is induced by inflammation, which leads to neurodegeneration. Disruption of the homeostasis of redox-active metals, iron and copper, is an integral part of the pathogenesis of Alzheimer’s disease and Parkinson’s disease. The developing neuroinflammation leads to intensification of the processes of peroxidation, oxidation of metals and the development of ferroptosis.

Journal

Advances in GerontologySpringer Journals

Published: Dec 1, 2022

Keywords: neuroinflammation; Parkinson’s disease; Alzheimer’s disease; COVID-19; microglia; APOE; ferroptosis; neurodegeneration

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