Cited by 1,750Alzheimer's disease research and treatmentsMitochondrial Function and PathologyDementia and Cognitive Impairment Research

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Oxidative Stress, Synaptic Dysfunction, and Alzheimer’s Disease

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Tönnies, Eric, Trushina, Eugenia·2017·Journal of Alzheimer s Disease

DOI 10.3233/jad-161088PMC PMC5409043

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Abstract

Alzheimer's disease (AD) is a devastating neurodegenerative disorder without a cure. Most AD cases are sporadic where age represents the greatest risk factor. Lack of understanding of the disease mechanism hinders the development of efficacious therapeutic approaches. The loss of synapses in the affected brain regions correlates best with cognitive impairment in AD patients and has been considered as the early mechanism that precedes neuronal loss. Oxidative stress has been recognized as a contributing factor in aging and in the progression of multiple neurodegenerative diseases including AD. Increased production of reactive oxygen species (ROS) associated with age- and disease-dependent loss of mitochondrial function, altered metal homeostasis, and reduced antioxidant defense directly affect synaptic activity and neurotransmission in neurons leading to cognitive dysfunction. In addition, molecular targets affected by ROS include nuclear and mitochondrial DNA, lipids, proteins, calcium homeostasis, mitochondrial dynamics and function, cellular architecture, receptor trafficking and endocytosis, and energy homeostasis. Abnormal cellular metabolism in turn could affect the production and accumulation of amyloid-β (Aβ) and hyperphosphorylated Tau protein, which independently could exacerbate mitochondrial dysfunction and ROS production, thereby contributing to a vicious cycle. While mounting evidence implicates ROS in the AD etiology, clinical trials with antioxidant therapies have not produced consistent results. In this review, we will discuss the role of oxidative stress in synaptic dysfunction in AD, innovative therapeutic strategies evolved based on a better understanding of the complexity of molecular mechanisms of AD, and the dual role ROS play in health and disease.

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Authors: Tönnies, E., & Trushina, E.
Affiliations: Mayo Clinic (US)
Corresponding author: Trushina, Eugenia
ORCID: Trushina, Eugenia
Venue: Journal of Alzheimer s Disease
Publisher: SAGE Publications
Published: 2017-04-19
Volume: 57
Issue: 4
Pages: 1105-1121
ISSN: 1387-2877 (ISSN-L)
1875-8908
DOI: 10.3233/jad-161088
PMC: PMC5409043
OpenAlex: W2568450381
Cited by: 1,750
References: 237
Citations by year: 2026: 135 · 2025: 220 · 2024: 259 · 2023: 258 · 2022: 253 · 2021: 246 · 2020: 193 · 2019: 101 · 2018: 54 · 2017: 30
FWCI: 12.72
Type: journal article
Language: en
Open access: bronze
doi.org
Licence: journals.sagepub.com/page/policies/text-and-data-mining-license (tdm)
Locations: Journal of Alzheimer s Disease (publishedVersion)
PubMed Central (publishedVersion, cc-by-nc)
PubMed (publishedVersion)
Funders: National Institutes of Health
National Institute on Aging (RF1AG055549)
National Institute of Environmental Health Sciences (R01ES020715)
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, oxidative stress
MeSH terms: Alzheimer Disease, Animals, Humans, Synapses, Oxidative Stress

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