Cited by 395Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

The DOI matches its Crossref record; 102 of the 104 references it cites were found in a registry or an index.

Abnormal mitochondrial dynamics and synaptic degeneration as early events in Alzheimer’s disease: Implications to mitochondria-targeted antioxidant therapeutics

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Reddy, P. Hemachandra, Tripathi, Raghav, Troung, Quang, Tirumala, Karuna, Reddy, Tejaswini P., Anekonda, Vishwanath, Shirendeb, Ulziibat P., Calkins, Marcus J., Reddy, Arubala P., Mao, Peizhong, Manczak, Maria·2012·Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease

Abstract

Synaptic pathology and mitochondrial oxidative damage are early events in Alzheimer's disease (AD) progression. Loss of synapses and synaptic damage are the best correlates of cognitive deficits found in AD patients. Recent research on amyloid beta (Aβ) and mitochondria in AD revealed that Aβ accumulates in synapses and synaptic mitochondria, leading to abnormal mitochondrial dynamics and synaptic degeneration in AD neurons. Further, recent studies using live-cell imaging and primary neurons from amyloid beta precursor protein (AβPP) transgenic mice revealed reduced mitochondrial mass, defective axonal transport of mitochondria and synaptic degeneration, indicating that Aβ is responsible for mitochondrial and synaptic deficiencies. Tremendous progress has been made in studying antioxidant approaches in mouse models of AD and clinical trials of AD patients. This article highlights the recent developments made in Aβ-induced abnormal mitochondrial dynamics, defective mitochondrial biogenesis, impaired axonal transport and synaptic deficiencies in AD. This article also focuses on mitochondrial approaches in treating AD, and also discusses latest research on mitochondria-targeted antioxidants in AD. This article is part of a Special Issue entitled: Antioxidants and Antioxidant Treatment in Disease.

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Crossref · 10.1016/j.bbadis.2011.10.011

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Metadata

Authors
Reddy, P. H., Tripathi, R., Troung, Q., Tirumala, K., Reddy, T. P., Anekonda, V., Shirendeb, U. P., Calkins, M. J., Reddy, A. P., Mao, P., & Manczak, M.
Affiliations
Oregon National Primate Research Center (US)
Corresponding author
Reddy, P. Hemachandra
Venue
Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease
Publisher
Elsevier BV
Published
2012-05
Volume
1822
Issue
5
Pages
639-649
ISSN
0925-4439 (ISSN-L)
OpenAlex
W1996981671
Cited by
394
References
104
Citations by year
2026: 29 · 2025: 17 · 2024: 22 · 2023: 27 · 2022: 30 · 2021: 38 · 2020: 29 · 2019: 30 · 2018: 26 · 2017: 36 · 2016: 31 · 2015: 19 · 2014: 31 · 2013: 18 · 2012: 10
FWCI
2.02
Type
journal article
Language
en
Open access
Locations
  • Biochimica et Biophysica Acta (BBA) - Molecular Basis of Disease (publishedVersion)
  • PubMed (publishedVersion)
  • Europe PMC (PubMed Central) (acceptedVersion)
  • PubMed Central (acceptedVersion)
Funders
  • NIH
  • Alzheimer Association
Topics
  • Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › 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
Alzheimer's disease, mitochondrial dynamics, synaptic degeneration, amyloid-beta, mitochondrial oxidative damage, mitochondrial biogenesis, mitochondria-targeted antioxidants, antioxidant therapeutics, synaptic mitochondria
MeSH terms
Alzheimer Disease, Animals, Antioxidants, Humans, Mice, Transgenic, Mitochondria, Synapses, Amyloid beta-Protein Precursor, Mice

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