title: Mitochondrial Dysfunction Contributes to the Pathogenesis of Alzheimer's Disease.
abstract: Alzheimer's disease (AD) is a neurodegenerative disease that affects millions of people worldwide. Currently, there is no effective treatment for AD, which indicates the necessity to understand the pathogenic mechanism of this disorder. Extracellular aggregates of amyloid precursor protein (APP), called Aβ peptide and neurofibrillary tangles (NFTs), formed by tau protein in the hyperphosphorylated form are considered the hallmarks of AD. Accumulative evidence suggests that tau pathology and Aβ affect neuronal cells compromising energy supply, antioxidant response, and synaptic activity. In this context, it has been showed that mitochondrial function could be affected by the presence of tau pathology and Aβ in AD. Mitochondria are essential for brain cells function and the improvement of mitochondrial activity contributes to preventing neurodegeneration. Several reports have suggested that mitochondria could be affected in terms of morphology, bioenergetics, and transport in AD. These defects affect mitochondrial health, which later will contribute to the pathogenesis of AD. In this review, we will discuss evidence that supports the importance of mitochondrial injury in the pathogenesis of AD and how studying these mechanisms could lead us to suggest new targets for diagnostic and therapeutic intervention against neurodegeneration.
authors.affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.
authors.forename: Fabian A
authors.initials: FA
authors.lastname: Cabezas-Opazo
authors.affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.
authors.forename: Katiana
authors.initials: K
authors.lastname: Vergara-Pulgar
authors.affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.
authors.forename: María José
authors.initials: MJ
authors.lastname: Pérez
authors.affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.
authors.forename: Claudia
authors.initials: C
authors.lastname: Jara
authors.affiliation: Departamento de Kinesiología, Universidad Metropolitana de Ciencias de la Educación, Ñuñoa, 7760197 Santiago, Chile.
authors.forename: Cesar
authors.initials: C
authors.lastname: Osorio-Fuentealba
authors.affiliation: Laboratory of Neurodegenerative Diseases, Centro de Investigación Biomédica, Universidad Autónoma de Chile, San Miguel, 8900000 Santiago, Chile.
authors.forename: Rodrigo A
authors.initials: RA
authors.lastname: Quintanilla
mesh_terms: D000544:Alzheimer Disease / Q000378:metabolism / Q000473:pathology*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D000818:Animals; D001369:Axons / Q000378:metabolism; D001921:Brain / Q000378:metabolism; D006801:Humans; D008928:Mitochondria / Q000378:metabolism*; D063154:Mitochondrial Dynamics; D016875:tau Proteins / Q000378:metabolism
chemical_list: D016229:Amyloid beta-Peptides; D016875:tau Proteins