ReviewFrontiers in synaptic neuroscience2025
Aging and Alzheimer's: the critical role of mitochondrial dysfunction and synaptic alterations.
Review in Frontiers in synaptic neuroscience, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
What it found
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
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Who cites it
5 citing papers in PubMed.
- Estrogen Withdrawal-Induced Cognitive Impairment in Menopausal Women: Mechanisms and Prospects for Integrated Interventions.International journal of molecular sciences · 2026Review
- Disrupting the Undruggable: Emerging Modalities for Targeting Protein-Protein Interactions in Oncology.Biology · 2026Review
- Simufilam in Alzheimer's Disease: Assessment of Efficacy of a Controversial Drug in Human Neuronal Cell Culture.Pharmaceuticals (Basel, Switzerland) · 2026Article
- Peripheral metabolomic profiling reveals lipid and amino acid alterations associated with immuno-inflammatory responses in treatment-naïve late-onset Alzheimer's disease.Frontiers in aging neuroscience · 2026Article
- Profiling arbutin as a potent cholinesterase and GSK-3β inhibitor and evaluating its cytotoxicity in SH-SY5Y cells for Alzheimer's disease therapy.Turkish journal of biology = Turk biyoloji dergisi · 2026Article
Corrections and comments
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Authors and funding
7 authors.
Funding
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Abstract
Alzheimer's disease is a progressive neurodegenerative disorder marked by cognitive decline, accumulation of amyloid-β plaques and neurofibrillary tangles, synaptic dysfunction, and mitochondrial impairment. Despite multiple therapeutic strategies, currently available treatments only provide symptomatic relief without halting disease progression. Emerging evidence implicates mitochondrial dysfunction-including oxidative stress, impaired calcium signaling, mitophagy deficits, disrupted proteostasis, and electron transport chain abnormalities, as central to AD pathogenesis. These dysfunctions contribute to synaptic degeneration, increased reactive oxygen species, and neuronal death. This review consolidates current knowledge on the mechanistic pathways of mitochondrial impairment in AD and their downstream effects on neuronal health. We also explore the therapeutic potential of multitarget approaches, including agents targeting Aβ and tau pathology, oxidative stress mitigation, mitochondrial quality control, and synaptic restoration. By integrating evidence from recent preclinical and clinical studies, this work highlights mitochondrial homeostasis as a promising frontier for disease-modifying therapies in AD.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.