Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration

Tau is an essential protein that physiologically promotes the assembly and stabilization of microtubules, and participates in neuronal development, axonal transport, and neuronal polarity. However, in a number of neurodegenerative diseases, including Alzheimer’s disease (AD), tau undergoes pathologi...

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Main Authors: María J. Pérez, Claudia Jara, Rodrigo A. Quintanilla
Format: Article
Language:English
Published: Frontiers Media S.A. 2018-07-01
Series:Frontiers in Neuroscience
Subjects:
Online Access:https://www.frontiersin.org/article/10.3389/fnins.2018.00441/full
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author María J. Pérez
María J. Pérez
Claudia Jara
Claudia Jara
Rodrigo A. Quintanilla
Rodrigo A. Quintanilla
author_facet María J. Pérez
María J. Pérez
Claudia Jara
Claudia Jara
Rodrigo A. Quintanilla
Rodrigo A. Quintanilla
author_sort María J. Pérez
collection DOAJ
description Tau is an essential protein that physiologically promotes the assembly and stabilization of microtubules, and participates in neuronal development, axonal transport, and neuronal polarity. However, in a number of neurodegenerative diseases, including Alzheimer’s disease (AD), tau undergoes pathological modifications in which soluble tau assembles into insoluble filaments, leading to synaptic failure and neurodegeneration. Mitochondria are responsible for energy supply, detoxification, and communication in brain cells, and important evidence suggests that mitochondrial failure could have a pivotal role in the pathogenesis of AD. In this context, our group and others investigated the negative effects of tau pathology on specific neuronal functions. In particular, we observed that the presence of these tau forms could affect mitochondrial function at three different levels: (i) mitochondrial transport, (ii) morphology, and (iii) bioenergetics. Therefore, mitochondrial dysfunction mediated by anomalous tau modifications represents a novel mechanism by which these forms contribute to the pathogenesis of AD. In this review, we will discuss the main results reported on pathological tau modifications and their effects on mitochondrial function and their importance for the synaptic communication and neurodegeneration.
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spelling doaj.art-d1013f9d7576419b9142da430a5c58b22022-12-22T02:53:41ZengFrontiers Media S.A.Frontiers in Neuroscience1662-453X2018-07-011210.3389/fnins.2018.00441369578Contribution of Tau Pathology to Mitochondrial Impairment in NeurodegenerationMaría J. Pérez0María J. Pérez1Claudia Jara2Claudia Jara3Rodrigo A. Quintanilla4Rodrigo A. Quintanilla5Laboratory of Neurodegenerative Diseases, Universidad Autónoma de Chile, Santiago, ChileCentro de Investigación y Estudio del Consumo de Alcohol en Adolescentes (CIAA), Santiago, ChileLaboratory of Neurodegenerative Diseases, Universidad Autónoma de Chile, Santiago, ChileCentro de Investigación y Estudio del Consumo de Alcohol en Adolescentes (CIAA), Santiago, ChileLaboratory of Neurodegenerative Diseases, Universidad Autónoma de Chile, Santiago, ChileCentro de Investigación y Estudio del Consumo de Alcohol en Adolescentes (CIAA), Santiago, ChileTau is an essential protein that physiologically promotes the assembly and stabilization of microtubules, and participates in neuronal development, axonal transport, and neuronal polarity. However, in a number of neurodegenerative diseases, including Alzheimer’s disease (AD), tau undergoes pathological modifications in which soluble tau assembles into insoluble filaments, leading to synaptic failure and neurodegeneration. Mitochondria are responsible for energy supply, detoxification, and communication in brain cells, and important evidence suggests that mitochondrial failure could have a pivotal role in the pathogenesis of AD. In this context, our group and others investigated the negative effects of tau pathology on specific neuronal functions. In particular, we observed that the presence of these tau forms could affect mitochondrial function at three different levels: (i) mitochondrial transport, (ii) morphology, and (iii) bioenergetics. Therefore, mitochondrial dysfunction mediated by anomalous tau modifications represents a novel mechanism by which these forms contribute to the pathogenesis of AD. In this review, we will discuss the main results reported on pathological tau modifications and their effects on mitochondrial function and their importance for the synaptic communication and neurodegeneration.https://www.frontiersin.org/article/10.3389/fnins.2018.00441/fulltaumitochondriaAlzheimer’s diseasesynapse neurodegenerationsynapsis
spellingShingle María J. Pérez
María J. Pérez
Claudia Jara
Claudia Jara
Rodrigo A. Quintanilla
Rodrigo A. Quintanilla
Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
Frontiers in Neuroscience
tau
mitochondria
Alzheimer’s disease
synapse neurodegeneration
synapsis
title Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
title_full Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
title_fullStr Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
title_full_unstemmed Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
title_short Contribution of Tau Pathology to Mitochondrial Impairment in Neurodegeneration
title_sort contribution of tau pathology to mitochondrial impairment in neurodegeneration
topic tau
mitochondria
Alzheimer’s disease
synapse neurodegeneration
synapsis
url https://www.frontiersin.org/article/10.3389/fnins.2018.00441/full
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