ArticleFrontiers in aging neuroscience2022
Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex.
Article in Frontiers in aging neuroscience, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 20 citations in OpenAlex.
- Revisiting Alzheimer's Disease Through the Somatostatin-Mitochondria Axis.Molecular neurobiology · 2026Review
- Article
- Extracellular vesicles from hiPSC-derived NSCs protect human neurons against Aβ-42 oligomers induced neurodegeneration, mitochondrial dysfunction and tau phosphorylation.Stem cell research & therapy · 2025Article
- Article
- Different amyloid β42 preparations induce different cell death pathways in the model of SH-SY5Y neuroblastoma cells.Cellular & molecular biology letters · 2024Article
- Article
- Targeting Mitochondrial Dysfunction and Reactive Oxygen Species for Neurodegenerative Disease Treatment.International journal of molecular sciences · 2024Review
- Biomarkers for Managing Neurodegenerative Diseases.Biomolecules · 2024Review
- Sex-dependent cholinergic effects on amyloid pathology: A translational study.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Mitochondrial Complex I and β-Amyloid Peptide Interplay in Alzheimer's Disease: A Critical Review of New and Old Little Regarded Findings.International journal of molecular sciences · 2023Review
- Exploring the role of mitochondria transfer/transplant and their long-non-coding RNAs in regenerative therapies for skin aging.Mitochondrion · 2023Article
- Protein Interactome of Amyloid-β as a Therapeutic Target.Pharmaceuticals (Basel, Switzerland) · 2023Review
- Mapping trends and hotspots of mitochondrial dysfunction in Alzheimer's disease from 2013 to 2022: a bibliometric analysis of global research.Frontiers in neuroscience · 2023Article
Corrections and comments
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Authors and funding
4 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing evidence suggests that mitochondrial dysfunction and aberrant release of mitochondrial reactive oxygen species (ROS) play crucial roles in early synaptic perturbations and neuropathology that drive memory deficits in Alzheimer's disease (AD). We recently showed that solubilized human amyloid beta peptide 1-42 (hAβ
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Registered trials
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