Mitochondrial dysfunction in Alzheimer’s disease: a proteomics perspective

Morteza Abyadeh; Vivek Gupta; Nitin Chitranshi; Veer Gupta; Yunqi Wu; Danit Saks; Roshana Vander Wall; Matthew J. Fitzhenry; Devaraj Basavarajappa; Yuyi You; Ghasem H. Salekdeh; Paul A. Haynes; Stuart L. Graham; Mehdi Mirzaei

doi:10.1080/14789450.2021.1918550

Mitochondrial dysfunction in Alzheimer’s disease: a proteomics perspective

Morteza Abyadeh, Vivek Gupta, Nitin Chitranshi, Veer Gupta, Yunqi Wu, Danit Saks, Roshana Vander Wall, Matthew J. Fitzhenry, Devaraj Basavarajappa, Yuyi You, Ghasem H. Salekdeh, Paul A. Haynes, Stuart L. Graham, Mehdi Mirzaei

Research output: Contribution to journal › Review article › peer-review

22 Citations (Scopus)

Abstract

Mitochondrial dysfunction is involved in Alzheimer’s disease (AD) pathogenesis. Mitochondria have their own genetic material; however, most of their proteins (∼99%) are synthesized as precursors on cytosolic ribosomes, and then imported into the mitochondria. Therefore, exploring proteome changes in these organelles can yield valuable information and shed light on the molecular mechanisms underlying mitochondrial dysfunction in AD. Here we review AD associated mitochondrial changes including the effects of amyloid beta and tau protein accumulation on the mitochondrial proteome. We also discuss the relationship of ApoE genetic polymorphism with mitochondrial changes, and present a meta-analysis of various differentially expressed proteins in the mitochondria in AD.

Original language	English
Pages (from-to)	295-304
Number of pages	10
Journal	Expert Review of Proteomics
Volume	18
Issue number	4
Early online date	3 May 2021
DOIs	https://doi.org/10.1080/14789450.2021.1918550
Publication status	Published - 2021

Keywords

Alzheimer’s disease
Mitochondrial dysfunction
Proteomics

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10.1080/14789450.2021.1918550

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title = "Mitochondrial dysfunction in Alzheimer{\textquoteright}s disease: a proteomics perspective",

abstract = "Mitochondrial dysfunction is involved in Alzheimer{\textquoteright}s disease (AD) pathogenesis. Mitochondria have their own genetic material; however, most of their proteins (∼99%) are synthesized as precursors on cytosolic ribosomes, and then imported into the mitochondria. Therefore, exploring proteome changes in these organelles can yield valuable information and shed light on the molecular mechanisms underlying mitochondrial dysfunction in AD. Here we review AD associated mitochondrial changes including the effects of amyloid beta and tau protein accumulation on the mitochondrial proteome. We also discuss the relationship of ApoE genetic polymorphism with mitochondrial changes, and present a meta-analysis of various differentially expressed proteins in the mitochondria in AD.",

keywords = "Alzheimer{\textquoteright}s disease, Mitochondrial dysfunction, Proteomics",

author = "Morteza Abyadeh and Vivek Gupta and Nitin Chitranshi and Veer Gupta and Yunqi Wu and Danit Saks and {Vander Wall}, Roshana and Fitzhenry, {Matthew J.} and Devaraj Basavarajappa and Yuyi You and Salekdeh, {Ghasem H.} and Haynes, {Paul A.} and Graham, {Stuart L.} and Mehdi Mirzaei",

year = "2021",

doi = "10.1080/14789450.2021.1918550",

language = "English",

volume = "18",

pages = "295--304",

journal = "Expert Review of Proteomics",

issn = "1478-9450",

publisher = "Expert Reviews Ltd.",

number = "4",

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TY - JOUR

T1 - Mitochondrial dysfunction in Alzheimer’s disease

T2 - a proteomics perspective

AU - Abyadeh, Morteza

AU - Gupta, Vivek

AU - Chitranshi, Nitin

AU - Gupta, Veer

AU - Wu, Yunqi

AU - Saks, Danit

AU - Vander Wall, Roshana

AU - Fitzhenry, Matthew J.

AU - Basavarajappa, Devaraj

AU - You, Yuyi

AU - Salekdeh, Ghasem H.

AU - Haynes, Paul A.

AU - Graham, Stuart L.

AU - Mirzaei, Mehdi

PY - 2021

Y1 - 2021

N2 - Mitochondrial dysfunction is involved in Alzheimer’s disease (AD) pathogenesis. Mitochondria have their own genetic material; however, most of their proteins (∼99%) are synthesized as precursors on cytosolic ribosomes, and then imported into the mitochondria. Therefore, exploring proteome changes in these organelles can yield valuable information and shed light on the molecular mechanisms underlying mitochondrial dysfunction in AD. Here we review AD associated mitochondrial changes including the effects of amyloid beta and tau protein accumulation on the mitochondrial proteome. We also discuss the relationship of ApoE genetic polymorphism with mitochondrial changes, and present a meta-analysis of various differentially expressed proteins in the mitochondria in AD.

AB - Mitochondrial dysfunction is involved in Alzheimer’s disease (AD) pathogenesis. Mitochondria have their own genetic material; however, most of their proteins (∼99%) are synthesized as precursors on cytosolic ribosomes, and then imported into the mitochondria. Therefore, exploring proteome changes in these organelles can yield valuable information and shed light on the molecular mechanisms underlying mitochondrial dysfunction in AD. Here we review AD associated mitochondrial changes including the effects of amyloid beta and tau protein accumulation on the mitochondrial proteome. We also discuss the relationship of ApoE genetic polymorphism with mitochondrial changes, and present a meta-analysis of various differentially expressed proteins in the mitochondria in AD.

KW - Alzheimer’s disease

KW - Mitochondrial dysfunction

KW - Proteomics

UR - http://www.scopus.com/inward/record.url?scp=85104960741&partnerID=8YFLogxK

U2 - 10.1080/14789450.2021.1918550

DO - 10.1080/14789450.2021.1918550

M3 - Review article

C2 - 33874826

VL - 18

SP - 295

EP - 304

JO - Expert Review of Proteomics

JF - Expert Review of Proteomics

SN - 1478-9450

IS - 4

ER -

Mitochondrial dysfunction in Alzheimer’s disease: a proteomics perspective

Abstract

Keywords

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