ArticleMolecular neurobiology2014
Mitochondrial toxic effects of Aβ through mitofusins in the early pathogenesis of Alzheimer's disease.
Article in Molecular neurobiology, 2014. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 papers.
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Who cites it
21 citing papers in PubMed, 32 citations in OpenAlex.
- Label-Free Detection of Cellular Aβ Accumulation and Mitochondrial Dysfunction in AD Cell Models via Raman Microscopy.Analytical chemistry · 2026Article
- Iron toxicity potentiates cell-type specific amyloid beta proteotoxicity inbioRxiv : the preprint server for biology · 2026Article
- Activation of GLP-1R ameliorates alcohol withdrawal induced anxiety-like behavior by regulating neuronal mitochondrial quality control.Frontiers in pharmacology · 2026Article
- Mitochondrial dynamics proteins as emerging drug targets.Trends in pharmacological sciences · 2023Review
- Biologically synthesized black ginger-selenium nanoparticle induces apoptosis and autophagy of AGS gastric cancer cells by suppressing the PI3K/Akt/mTOR signaling pathway.Journal of nanobiotechnology · 2022Article
- Reduced VDAC1, Maintained Mitochondrial Dynamics and Enhanced Mitochondrial Biogenesis in a Transgenic Tau Mouse Model of Alzheimer's Disease.International journal of molecular sciences · 2022Article
- A partial reduction of VDAC1 enhances mitophagy, autophagy, synaptic activities in a transgenic Tau mouse model.Aging cell · 2022Article
- Nuclear and Cytoplasmatic Players in Mitochondria-Related CNS Disorders: Chromatin Modifications and Subcellular Trafficking.Biomolecules · 2022Review
- Age-Dependent Behavioral and Metabolic Assessment ofFrontiers in molecular neuroscience · 2022Article
- Mitophagy and Oxidative Stress: The Role of Aging.Antioxidants (Basel, Switzerland) · 2021Review
- High-Resolution Respirometry in Assessment of Mitochondrial Function in Neuroblastoma SH-SY5Y Intact Cells.The Journal of membrane biology · 2020Article
- Nicotinamide phosphoribosyltransferase‑related signaling pathway in early Alzheimer's disease mouse models.Molecular medicine reports · 2019Article
- Ferroportin disease mutations influence manganese accumulation and cytotoxicity.FASEB journal : official publication of the Federation of American Societies for Experimental Biology · 2019Article
- Putrescine as indicator of manganese neurotoxicity: Dose-response study in human SH-SY5Y cells.Food and chemical toxicology : an international journal published for the British Industrial Biological Research Association · 2018Article
- Association of Tea Consumption with Risk of Alzheimer's Disease and Anti-Beta-Amyloid Effects of Tea.Nutrients · 2018Review
- Mitofusin 2: from functions to disease.Cell death & disease · 2018Review
- Mitochondrial dysfunction in the APP/PSEN1 mouse model of Alzheimer's disease and a novel protective role for ascorbate.Free radical biology & medicine · 2017Article
- From the Cover: Manganese Stimulates Mitochondrial H2O2 Production in SH-SY5Y Human Neuroblastoma Cells Over Physiologic as well as Toxicologic Range.Toxicological sciences : an official journal of the Society of Toxicology · 2017Article
- Review
- The effects of endogenous non-peptide molecule isatin and hydrogen peroxide on proteomic profiling of rat brain amyloid-β binding proteins: relevance to Alzheimer's disease?International journal of molecular sciences · 2014Article
Corrections and comments
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Authors and funding
5 authors at 4 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction has been implicated in the pathogenesis of Alzheimer's disease (AD). However, it is obscure how amyloid-beta (Aβ) can impair mitochondria in the early stage of AD pathology. Using PrP-hAPP/hPS1 double-transgenic AD mouse model, we find that abnormal mitochondrial morphology and damaged mitochondrial structure in hippocampal neurons appear in the early stage of AD-like disease development. We also find consistent mitochondrial abnormalities in the SH-SY5Y cells, which express amyloid precursor protein (APP) Swedish mutation (APPsw) and have been used as a cell model of the early-onset AD. Significant changes of mitofusin GTPases (Mfn1 and Mfn2) were detected both in the PrP-hAPP/hPS1 brains and SH-SY5Y cells. Moreover, our results show that Aβ accumulation in neurons of PrP-hAPP/hPS1 mice can affect the neurogenesis prior to plaque formation. These findings suggest that mitochondrial impairment is a very early event in AD pathogenesis and abnormal expression of Mfn1 and Mfn2 caused by excessive intracellular Aβ is the possible molecular mechanism. Interestingly, L-theanine has significant effects on regulating mitochondrial fusion proteins in SH-SY5Y (APPsw) cells. Overall, our results not only suggest a new early mechanism of AD pathogenesis but also propose a preventive candidate, L-theanine, for the treatment of AD.
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