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Early-Life Environment Influence on Late-Onset Alzheimer’s Disease
With the expand of the population’s average age, the incidence of neurodegenerative disorders has dramatically increased over the last decades. Alzheimer disease (AD) which is the most prevalent neurodegenerative disease is mostly sporadic and primarily characterized by cognitive deficits and neurop...
Autores principales: | , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
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Frontiers Media S.A.
2022
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8891536/ https://www.ncbi.nlm.nih.gov/pubmed/35252195 http://dx.doi.org/10.3389/fcell.2022.834661 |
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author | Gauvrit, Thibaut Benderradji, Hamza Buée, Luc Blum, David Vieau, Didier |
author_facet | Gauvrit, Thibaut Benderradji, Hamza Buée, Luc Blum, David Vieau, Didier |
author_sort | Gauvrit, Thibaut |
collection | PubMed |
description | With the expand of the population’s average age, the incidence of neurodegenerative disorders has dramatically increased over the last decades. Alzheimer disease (AD) which is the most prevalent neurodegenerative disease is mostly sporadic and primarily characterized by cognitive deficits and neuropathological lesions such as amyloid -β (Aβ) plaques and neurofibrillary tangles composed of hyper- and/or abnormally phosphorylated Tau protein. AD is considered a complex disease that arises from the interaction between environmental and genetic factors, modulated by epigenetic mechanisms. Besides the well-described cognitive decline, AD patients also exhibit metabolic impairments. Metabolic and cognitive perturbations are indeed frequently observed in the Developmental Origin of Health and Diseases (DOHaD) field of research which proposes that environmental perturbations during the perinatal period determine the susceptibility to pathological conditions later in life. In this review, we explored the potential influence of early environmental exposure to risk factors (maternal stress, malnutrition, xenobiotics, chemical factors … ) and the involvement of epigenetic mechanisms on the programming of late-onset AD. Animal models indicate that offspring exposed to early-life stress during gestation and/or lactation increase both AD lesions, lead to defects in synaptic plasticity and finally to cognitive impairments. This long-lasting epigenetic programming could be modulated by factors such as nutriceuticals, epigenetic modifiers or psychosocial behaviour, offering thus future therapeutic opportunity to protect from AD development. |
format | Online Article Text |
id | pubmed-8891536 |
institution | National Center for Biotechnology Information |
language | English |
publishDate | 2022 |
publisher | Frontiers Media S.A. |
record_format | MEDLINE/PubMed |
spelling | pubmed-88915362022-03-04 Early-Life Environment Influence on Late-Onset Alzheimer’s Disease Gauvrit, Thibaut Benderradji, Hamza Buée, Luc Blum, David Vieau, Didier Front Cell Dev Biol Cell and Developmental Biology With the expand of the population’s average age, the incidence of neurodegenerative disorders has dramatically increased over the last decades. Alzheimer disease (AD) which is the most prevalent neurodegenerative disease is mostly sporadic and primarily characterized by cognitive deficits and neuropathological lesions such as amyloid -β (Aβ) plaques and neurofibrillary tangles composed of hyper- and/or abnormally phosphorylated Tau protein. AD is considered a complex disease that arises from the interaction between environmental and genetic factors, modulated by epigenetic mechanisms. Besides the well-described cognitive decline, AD patients also exhibit metabolic impairments. Metabolic and cognitive perturbations are indeed frequently observed in the Developmental Origin of Health and Diseases (DOHaD) field of research which proposes that environmental perturbations during the perinatal period determine the susceptibility to pathological conditions later in life. In this review, we explored the potential influence of early environmental exposure to risk factors (maternal stress, malnutrition, xenobiotics, chemical factors … ) and the involvement of epigenetic mechanisms on the programming of late-onset AD. Animal models indicate that offspring exposed to early-life stress during gestation and/or lactation increase both AD lesions, lead to defects in synaptic plasticity and finally to cognitive impairments. This long-lasting epigenetic programming could be modulated by factors such as nutriceuticals, epigenetic modifiers or psychosocial behaviour, offering thus future therapeutic opportunity to protect from AD development. Frontiers Media S.A. 2022-02-17 /pmc/articles/PMC8891536/ /pubmed/35252195 http://dx.doi.org/10.3389/fcell.2022.834661 Text en Copyright © 2022 Gauvrit, Benderradji, Buée, Blum and Vieau. https://creativecommons.org/licenses/by/4.0/This is an open-access article distributed under the terms of the Creative Commons Attribution License (CC BY). The use, distribution or reproduction in other forums is permitted, provided the original author(s) and the copyright owner(s) are credited and that the original publication in this journal is cited, in accordance with accepted academic practice. No use, distribution or reproduction is permitted which does not comply with these terms. |
spellingShingle | Cell and Developmental Biology Gauvrit, Thibaut Benderradji, Hamza Buée, Luc Blum, David Vieau, Didier Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title | Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title_full | Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title_fullStr | Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title_full_unstemmed | Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title_short | Early-Life Environment Influence on Late-Onset Alzheimer’s Disease |
title_sort | early-life environment influence on late-onset alzheimer’s disease |
topic | Cell and Developmental Biology |
url | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8891536/ https://www.ncbi.nlm.nih.gov/pubmed/35252195 http://dx.doi.org/10.3389/fcell.2022.834661 |
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