ArticleNeuroreport2017
Mitochondrial dynamics changes with age in an APPsw/PS1dE9 mouse model of Alzheimer's disease.
Article in Neuroreport, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 1 of them a synthesis that pooled it.
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Who cites it
30 citing papers in PubMed, 1 synthesis or guideline pooled it, 51 citations in OpenAlex.
- Ferulic Acid in Animal Models of Alzheimer's Disease: A Systematic Review of Preclinical Studies.Cells · 2021Pooled it
- The central role of mitochondrial dysfunction in neurodegeneration: implications for therapy.Molecular and cellular biochemistry · 2026Review
- Mitochondrial Dysfunction in Alzheimer's Disease and Mitochondria-Targeted Therapeutics.Cells · 2026Review
- Digging Deep into Alzheimer Disease: How Electron Microscopy Helps Elucidating Its Pathogenesis.Cellular and molecular neurobiology · 2026Review
- Features of Mitochondrial Dynamics in Different Brain Parts of Patients with Alzheimer's Disease.International journal of molecular sciences · 2025Article
- Insights into the molecular mechanism of neurological diseases and their pathophysiological responses.Archives of toxicology · 2025Review
- Mitochondria-Associated Membrane Dysfunction in Neurodegeneration and Its Effects on Lipid Metabolism, Calcium Signaling, and Cell Fate.Membranes · 2025Review
- Cannabidiolic Acid Rescues Deficits in Hippocampal Long-Term Potentiation in Models of Alzheimer's Disease: An Electrophysiological and Proteomic Analysis.International journal of molecular sciences · 2025Article
- Mitochondrial Dynamics in Brain Cells During Normal and Pathological Aging.International journal of molecular sciences · 2024Review
- MAMs and Mitochondrial Quality Control: Overview and Their Role in Alzheimer's Disease.Neurochemical research · 2024Review
- Promoting Alzheimer's disease research and therapy with stem cell technology.Stem cell research & therapy · 2024Review
- Mitochondrial dysfunction in Alzheimer's disease: a key frontier for future targeted therapies.Frontiers in immunology · 2024Review
- Maintenance of mitochondrial homeostasis for Alzheimer's disease: Strategies and challenges.Redox biology · 2023Review
- CEND1 deficiency induces mitochondrial dysfunction and cognitive impairment in Alzheimer's disease.Cell death and differentiation · 2022Article
- Amyloid-β impairs mitochondrial dynamics and autophagy in Alzheimer's disease experimental models.Scientific reports · 2022Article
- Alterations in hippocampal mitochondrial dynamics are associated with neurodegeneration and recognition memory decline in old male mice.Biogerontology · 2022Article
- Regulation of mitochondrial dysfunction induced cell apoptosis is a potential therapeutic strategy for herbal medicine to treat neurodegenerative diseases.Frontiers in pharmacology · 2022Review
- A Review of ApoE4 Interference Targeting Mitophagy Molecular Pathways for Alzheimer's Disease.Frontiers in aging neuroscience · 2022Review
- Impact prediction of translocation of the mitochondrial outer membrane 70 as biomarker in Alzheimer's disease.Frontiers in aging neuroscience · 2022Article
- Contribution of Mitochondrial Dysfunction Combined with NLRP3 Inflammasome Activation in Selected Neurodegenerative Diseases.Pharmaceuticals (Basel, Switzerland) · 2021Review
Corrections and comments
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Authors and funding
9 authors at 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Increasing research suggests that mitochondrial defects play a major role in Alzheimer's disease (AD) pathogenesis. We aimed to better understand changes in mitochondria with the development and progression of AD. We compared APPsw/PS1dE9 transgenic mice at 3, 6, 9, and 12 months old as an animal model of AD and age-matched C57BL/6 mice as controls. The learning ability and spatial memory ability of APPsw/PS1dE9 mice showed significant differences compared with controls until 9 and 12 months. Mitochondrial morphology was altered in hippocampus tissue of APPsw/PS1dE9 mice beginning from the third month. 'Medullary corpuscle', which is formed by the accumulation of a large amount of degenerative and fragmented mitochondria in neuropils, may be the characteristic change observed on electron microscopy at a late stage of AD. Moreover, levels of mitochondrial fusion proteins (optic atrophy 1 and mitofusin 2) and fission proteins (dynamin-related protein 1 and fission 1) were altered in transgenic mice compared with controls with progression of AD. We found increased levels of fission and fusion proteins in APP/PS1 mice at 3 months, indicating that the presence of abnormal mitochondrial dynamics may be events in early AD progression. Changes in mitochondrial preceded the onset of memory decline as measured by the modified Morris water maze test. Abnormal mitochondrial dynamics could be a marker for early diagnosis of AD and monitoring disease progression. Further research is needed to study the signaling pathways that govern mitochondrial fission/fusion in AD.
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