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Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice

Old age is a risk factor for Alzheimer’s disease (AD), which is characterized by hippocampal impairment together with substantial changes in glial cell functions. Are these alterations due to the disease progression or are they a consequence of aging? To start addressing this issue, we studied the e...

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Autores principales: Bronzuoli, Maria Rosanna, Facchinetti, Roberta, Valenza, Marta, Cassano, Tommaso, Steardo, Luca, Scuderi, Caterina
Formato: Online Artículo Texto
Lenguaje:English
Publicado: Frontiers Media S.A. 2019
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6562169/
https://www.ncbi.nlm.nih.gov/pubmed/31244658
http://dx.doi.org/10.3389/fphar.2019.00644
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author Bronzuoli, Maria Rosanna
Facchinetti, Roberta
Valenza, Marta
Cassano, Tommaso
Steardo, Luca
Scuderi, Caterina
author_facet Bronzuoli, Maria Rosanna
Facchinetti, Roberta
Valenza, Marta
Cassano, Tommaso
Steardo, Luca
Scuderi, Caterina
author_sort Bronzuoli, Maria Rosanna
collection PubMed
description Old age is a risk factor for Alzheimer’s disease (AD), which is characterized by hippocampal impairment together with substantial changes in glial cell functions. Are these alterations due to the disease progression or are they a consequence of aging? To start addressing this issue, we studied the expression of specific astrocytic and microglial structural and functional proteins in a validated transgenic model of AD (3×Tg-AD). These mice develop both amyloid plaques and neurofibrillary tangles, and initial signs of the AD-like pathology have been documented as early as three months of age. We compared male 3×Tg-AD mice at 6 and 12 months of age with their wild-type age-matched counterparts. We also investigated neurons by examining the expression of both the microtubule-associated protein 2 (MAP2), a neuronal structural protein, and the brain-derived neurotrophic factor (BDNF). The latter is indeed a crucial indicator for synaptic plasticity and neurogenesis/neurodegeneration. Our results show that astrocytes are more susceptible to aging than microglia, regardless of mouse genotype. Moreover, we discovered significant age-dependent alterations in the expression of proteins responsible for astrocyte–astrocyte and astrocyte–neuron communication, as well as a significant age-dependent decline in BDNF expression. Our data promote further research on the unexplored role of astroglia in both physiological and pathological aging.
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spelling pubmed-65621692019-06-26 Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice Bronzuoli, Maria Rosanna Facchinetti, Roberta Valenza, Marta Cassano, Tommaso Steardo, Luca Scuderi, Caterina Front Pharmacol Pharmacology Old age is a risk factor for Alzheimer’s disease (AD), which is characterized by hippocampal impairment together with substantial changes in glial cell functions. Are these alterations due to the disease progression or are they a consequence of aging? To start addressing this issue, we studied the expression of specific astrocytic and microglial structural and functional proteins in a validated transgenic model of AD (3×Tg-AD). These mice develop both amyloid plaques and neurofibrillary tangles, and initial signs of the AD-like pathology have been documented as early as three months of age. We compared male 3×Tg-AD mice at 6 and 12 months of age with their wild-type age-matched counterparts. We also investigated neurons by examining the expression of both the microtubule-associated protein 2 (MAP2), a neuronal structural protein, and the brain-derived neurotrophic factor (BDNF). The latter is indeed a crucial indicator for synaptic plasticity and neurogenesis/neurodegeneration. Our results show that astrocytes are more susceptible to aging than microglia, regardless of mouse genotype. Moreover, we discovered significant age-dependent alterations in the expression of proteins responsible for astrocyte–astrocyte and astrocyte–neuron communication, as well as a significant age-dependent decline in BDNF expression. Our data promote further research on the unexplored role of astroglia in both physiological and pathological aging. Frontiers Media S.A. 2019-06-06 /pmc/articles/PMC6562169/ /pubmed/31244658 http://dx.doi.org/10.3389/fphar.2019.00644 Text en Copyright © 2019 Bronzuoli, Facchinetti, Valenza, Cassano, Steardo and Scuderi http://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 Pharmacology
Bronzuoli, Maria Rosanna
Facchinetti, Roberta
Valenza, Marta
Cassano, Tommaso
Steardo, Luca
Scuderi, Caterina
Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title_full Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title_fullStr Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title_full_unstemmed Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title_short Astrocyte Function Is Affected by Aging and Not Alzheimer’s Disease: A Preliminary Investigation in Hippocampi of 3xTg-AD Mice
title_sort astrocyte function is affected by aging and not alzheimer’s disease: a preliminary investigation in hippocampi of 3xtg-ad mice
topic Pharmacology
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6562169/
https://www.ncbi.nlm.nih.gov/pubmed/31244658
http://dx.doi.org/10.3389/fphar.2019.00644
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