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J Alzheimers Dis. 2010;20 Suppl 2:S499-512. doi: 10.3233/JAD-2010-100504.

Amyloid-beta and mitochondria in aging and Alzheimer's disease: implications for synaptic damage and cognitive decline.

Author information

1
Neurogenetics Laboratory, Division of Neuroscience, Oregon National Primate Research Center, Beaverton, OR, USA. reddyh@ohsu.edu

Abstract

This article reviews the role of amyloid-beta (Abeta) and mitochondria in synaptic damage and cognitive decline found in patients with Alzheimer's disease (AD). Recent molecular, cellular, animal model, and postmortem brain studies have revealed that Abeta and mitochondrial abnormalities are key factors that cause synaptic damage and cognitive decline in AD. Abeta is reported to accumulate in subcellular compartments and to impair the normal function of neurons in AD patients. Further, recent studies using biochemical methods and electron microscopy have revealed that the accumulation of Abeta at nerve terminals affect synaptic activities, including the release of neurotransmitters and synaptic vesicles. Recent studies of the relationship between mitochondria and Abeta in AD patients suggest that in mitochondria, structural changes caused by Abeta result in increased mitochondrial fragmentation, decreased mitochondrial fusion, mitochondrial dysfunction, and synaptic damage. This paper discusses the latest research on Abeta, mitochondria, age-dependent factors of AD in the brain, and synaptic damage in AD. This paper also briefly discusses potential mitochondrial therapeutics in the treatment of patients with AD.

PMID:
20413847
PMCID:
PMC3059092
DOI:
10.3233/JAD-2010-100504
[Indexed for MEDLINE]
Free PMC Article

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