Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis

Pavel F Pavlov; Anna Camilla Hansson Petersen; Elzbieta Glaser; Maria Ankarcrona

doi:10.1111/j.1582-4934.2009.00892.x

Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis

Pavel F Pavlov, Anna Camilla Hansson Petersen, Elzbieta Glaser, Maria Ankarcrona

45 Citationer (Scopus)

Abstract

Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.

Originalsprog	Engelsk
Tidsskrift	Journal of Cellular and Molecular Medicine
Vol/bind	13
Udgave nummer	10
Sider (fra-til)	4137-45
Antal sider	9
ISSN	1582-1838
DOI	https://doi.org/10.1111/j.1582-4934.2009.00892.x
Status	Udgivet - 2009

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10.1111/j.1582-4934.2009.00892.x

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title = "Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis",

abstract = "Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.",

keywords = "Aging, Alzheimer Disease, Amyloid beta-Protein Precursor, Animals, Brain, Humans, Mitochondria, Organ Specificity",

author = "Pavlov, {Pavel F} and Petersen, {Anna Camilla Hansson} and Elzbieta Glaser and Maria Ankarcrona",

year = "2009",

doi = "10.1111/j.1582-4934.2009.00892.x",

language = "English",

volume = "13",

pages = "4137--45",

journal = "Journal of Cellular and Molecular Medicine",

issn = "1582-1838",

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TY - JOUR

T1 - Mitochondrial accumulation of APP and Abeta

T2 - significance for Alzheimer disease pathogenesis

AU - Pavlov, Pavel F

AU - Petersen, Anna Camilla Hansson

AU - Glaser, Elzbieta

AU - Ankarcrona, Maria

PY - 2009

Y1 - 2009

N2 - Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.

AB - Accumulating evidence suggest that alterations in energy metabolism are among the earliest events that occur in the Alzheimer disease (AD) affected brain. Energy consumption is drastically decreased in the AD-affected regions of cerebral cortex and hippocampus pointing towards compromised mitochondrial function of neurons within specific brain regions. This is accompanied by an elevated production of reactive oxygen species contributing to increased rates of neuronal loss in the AD-affected brain regions. In this review, we will discuss the role of mitochondrial function and dysfunction in AD. We will focus on the consequences of amyloid precursor protein and amyloid-beta peptide accumulation in mitochondria and their involvement in AD pathogenesis.

KW - Aging

KW - Alzheimer Disease

KW - Amyloid beta-Protein Precursor

KW - Animals

KW - Brain

KW - Humans

KW - Mitochondria

KW - Organ Specificity

U2 - 10.1111/j.1582-4934.2009.00892.x

DO - 10.1111/j.1582-4934.2009.00892.x

M3 - Journal article

C2 - 19725915

SN - 1582-1838

VL - 13

SP - 4137

EP - 4145

JO - Journal of Cellular and Molecular Medicine

JF - Journal of Cellular and Molecular Medicine

IS - 10

ER -

Mitochondrial accumulation of APP and Abeta: significance for Alzheimer disease pathogenesis

Abstract

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