Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

P. Hemachandra Reddy; M. Flint Beal

doi:10.1016/j.molmed.2007.12.002

Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

P. Hemachandra Reddy
, M. Flint Beal

Research output: Contribution to journal › Article › peer-review

907 Scopus citations

Abstract

Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic mouse models of AD suggest that oxidative damage, induced by amyloid β (Aβ), is associated with mitochondria early in AD progression. Aβ and amyloid-precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron-transport chain, increase reactive oxygen species production, cause mitochondrial damage and prevent neurons from functioning normally. Furthermore, accumulation of Aβ at synaptic terminals might contribute to synaptic damage and cognitive decline in patients with AD. Here, we describe recent studies regarding the roles of Aβ and mitochondrial function in AD progression and particularly in synaptic damage and cognitive decline.

Original language	English (US)
Pages (from-to)	45-53
Number of pages	9
Journal	Trends in Molecular Medicine
Volume	14
Issue number	2
DOIs	https://doi.org/10.1016/j.molmed.2007.12.002
State	Published - Feb 2008

Funding

Our sincere apologies to all whose work could not be cited owing to space restrictions. This article is supported by grants from KaloBios Pharmaceuticals, Inc. and the National Institutes of Health (AG028072 and AG026051).

Funders	Funder number
KaloBios Pharmaceuticals Inc.
Author National Institutes of Health National Institutes of Health National Institutes of Health National Institutes of Health The Bev Hartig Huntington's Disease Foundation National Institutes of Health	AG026051
National Institute of Aging	R01AG028072

ASJC Scopus subject areas

Molecular Medicine
Molecular Biology

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10.1016/j.molmed.2007.12.002

Cite this

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abstract = "Recent studies of postmortem brains from Alzheimer's disease (AD) patients and transgenic mouse models of AD suggest that oxidative damage, induced by amyloid β (Aβ), is associated with mitochondria early in AD progression. Aβ and amyloid-precursor protein are known to localize to mitochondrial membranes, block the transport of nuclear-encoded mitochondrial proteins to mitochondria, interact with mitochondrial proteins, disrupt the electron-transport chain, increase reactive oxygen species production, cause mitochondrial damage and prevent neurons from functioning normally. Furthermore, accumulation of Aβ at synaptic terminals might contribute to synaptic damage and cognitive decline in patients with AD. Here, we describe recent studies regarding the roles of Aβ and mitochondrial function in AD progression and particularly in synaptic damage and cognitive decline.",

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Amyloid beta, mitochondrial dysfunction and synaptic damage: implications for cognitive decline in aging and Alzheimer's disease

Abstract

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