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Mitochondrial bioenergetics is altered in fibroblasts from patients with sporadic Alzheimer's disease

dc.contributor.authorPérez M.J.
dc.contributor.authorPonce D.P.
dc.contributor.authorOsorio-Fuentealba C.
dc.contributor.authorBehrens M.I.
dc.contributor.authorQuintanilla R.A.
dc.date.accessioned2020-09-02T22:25:46Z
dc.date.available2020-09-02T22:25:46Z
dc.date.issued2017
dc.identifier10.3389/fnins.2017.00553
dc.identifier.citation11, OCT, -
dc.identifier.issn16624548
dc.identifier.urihttps://hdl.handle.net/20.500.12728/5772
dc.descriptionThe identification of an early biomarker to diagnose Alzheimer's disease (AD) remains a challenge. Neuropathological studies in animal and AD patients have shown that mitochondrial dysfunction is a hallmark of the development of the disease. Current studies suggest the use of peripheral tissues, like skin fibroblasts as a possibility to detect the early pathological alterations present in the AD brain. In this context, we studied mitochondrial function properties (bioenergetics and morphology) in cultured fibroblasts obtained from AD, aged-match and young healthy patients. We observed that AD fibroblasts presented a significant reduction in mitochondrial length with important changes in the expression of proteins that control mitochondrial fusion. Moreover, AD fibroblasts showed a distinct alteration in proteolytic processing of OPA1, a master regulator of mitochondrial fusion, compared to control fibroblasts. Complementary to these changes AD fibroblasts showed a dysfunctional mitochondrial bioenergetics profile that differentiates these cells from aged-matched and young patient fibroblasts. Our findings suggest that the human skin fibroblasts obtained from AD patients could replicate mitochondrial impairment observed in the AD brain. These promising observations suggest that the analysis of mitochondrial bioenergetics could represent a promising strategy to develop new diagnostic methods in peripheral tissues of AD patients. © 2017 Pérez, Ponce, Osorio-Fuentealba, Behrens and Quintanilla.
dc.language.isoen
dc.publisherFrontiers Media S.A.
dc.subjectAlzheimer's disease
dc.subjectBiomarker
dc.subjectFibroblasts
dc.subjectMitochondria
dc.subjectOPA1
dc.subjectoptic atrophy 1 protein
dc.subjectregulator protein
dc.subjectunclassified drug
dc.subjectadult
dc.subjectaged
dc.subjectAlzheimer disease
dc.subjectArticle
dc.subjectbioenergy
dc.subjectbrain mitochondrion
dc.subjectcell fusion
dc.subjectcell structure
dc.subjectcontrolled study
dc.subjectdiagnostic test
dc.subjectdisease marker
dc.subjectdisorders of mitochondrial functions
dc.subjecthuman
dc.subjecthuman cell
dc.subjecthuman cell culture
dc.subjectmiddle aged
dc.subjectprotein degradation
dc.subjectprotein expression
dc.subjectprotein processing
dc.subjectskin fibroblast
dc.subjectvery elderly
dc.titleMitochondrial bioenergetics is altered in fibroblasts from patients with sporadic Alzheimer's disease
dc.typeArticle


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