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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...

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Autores principales: Gauvrit, Thibaut, Benderradji, Hamza, Buée, Luc, Blum, David, Vieau, Didier
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2022
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.
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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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