Cited by 95Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

Amyloid precursor protein and mitochondrial dysfunction in Alzheimer's disease

Anandatheerthavarada, Hindupur K., Devi, Latha·2007·The Neuroscientist

Abstract

Growing evidence suggests that mitochondrial dysfunction is one of the key intracellular lesions associated with the pathogenesis of Alzheimer's disease (AD). Mitochondria, the powerhouses of the cell, participate in a number of physiological functions that include calcium homeostasis, signal transduction, and apoptosis. However, the pathophysiological mechanisms underlying the decline of mitochondrial vital functions leading to the dysfunction of mitochondria during AD are not well understood. Recent literature has observed the accumulation of Alzheimer's amyloid precursor protein (APP) and its C-terminal-cleaved product beta-amyloid (Abeta) in the mitochondrial compartment. Furthermore, evidence also implicates that the accumulation of full-length APP and Abeta in the mitochondrial compartment has a causative role in impairing mitochondrial physiological functions. Here, we review the mode of mitochondrial transport of full-length APP and Abeta and its pathological implications in bringing about mitochondrial dysfunction as seen in AD.

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Crossref · 10.1177/1073858407303536

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Authors
Anandatheerthavarada, H. K., & Devi, L.
Affiliations
University of Pennsylvania (US)
Corresponding author
Anandatheerthavarada, Hindupur K.
Venue
The Neuroscientist
Published
2007-12
Volume
13
Issue
6
Pages
626-638
ISSN
  • 1073-8584 (ISSN-L)
  • 1089-4098
OpenAlex
W2071803058
Cited by
95
References
69
Citations by year
2026: 3 · 2024: 1 · 2023: 4 · 2022: 7 · 2021: 5 · 2020: 8 · 2019: 3 · 2018: 5 · 2017: 8 · 2016: 5 · 2015: 3 · 2014: 5 · 2013: 4 · 2012: 4
FWCI
0.97
Type
journal article
Language
en
Open access
closed
Locations
  • The Neuroscientist (publishedVersion)
  • PubMed (publishedVersion)
Funders
National Institute on Aging (R01AG021920, AG 021920)
Topics
  • Health Sciences › Medicine › Physiology › Alzheimer's disease research and treatments
  • Life Sciences › Biochemistry, Genetics and Molecular Biology › Molecular Biology › Mitochondrial Function and Pathology
  • Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords
amyloid precursor protein, mitochondrial dysfunction, Alzheimer's disease, amyloid-beta, mitochondrial transport, calcium homeostasis, apoptosis
MeSH terms
Alzheimer Disease, Animals, Humans, Mitochondria, Models, Biological, Amyloid beta-Protein Precursor, Mitochondrial Diseases

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