ArticleAging cell2022
A synapsin Ⅰ cleavage fragment contributes to synaptic dysfunction in Alzheimer's disease.
Article in Aging cell, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 14 papers.
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14 citing papers in PubMed, 39 citations in OpenAlex.
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- Cholestanol promotes tau pathology in a mouse model of tauopathy.Cellular and molecular life sciences : CMLS · 2025Article
- Association of qEEG TAR and TBR During Eyes-Open and Eyes-Closed with Plasma Oligomeric Amyloid-β Levels in an Aging Population.Journal of clinical medicine · 2025Article
- Biomarkers of mature neuronal differentiation and related diseases.Future science OA · 2024Review
- Effect of Kruppel-like factor 4 on PTZ-induced acute seizure mice.Journal of cellular and molecular medicine · 2024Article
- Neuroprotection by Polyherbal Medicine Divya-Medha-Vati Against Scopolamine-Induced Cognitive Impairment Through Modulation of Oxidative Stress, Acetylcholine Activity, and Cell Signaling.Molecular neurobiology · 2024Article
- AEP-cleaved DDX3X induces alternative RNA splicing events to mediate cancer cell adaptation in harsh microenvironments.The Journal of clinical investigation · 2023Article
- Cholestanol accelerates α-synuclein aggregation and spreading by activating asparagine endopeptidase.JCI insight · 2023Article
- Supraphysiologic doses of 17β-estradiol aggravate depression-like behaviors in ovariectomized mice possibly via regulating microglial responses and brain glycerophospholipid metabolism.Journal of neuroinflammation · 2023Article
- Damaged mitochondria coincide with presynaptic vesicle loss and abnormalities in alzheimer's disease brain.Acta neuropathologica communications · 2023Article
- Phrenic nerve stimulation mitigates hippocampal and brainstem inflammation in an ARDS model.Frontiers in physiology · 2023Article
- A synapsin Ⅰ cleavage fragment contributes to synaptic dysfunction in Alzheimer's disease.Aging cell · 2022Article
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Authors and funding
12 authors at 2 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synaptic dysfunction is a key feature of Alzheimer's disease (AD). However, the molecular mechanisms underlying synaptic dysfunction remain unclear. Here, we show that synapsin Ⅰ, one of the most important synaptic proteins, is fragmented by the cysteine proteinase asparagine endopeptidase (AEP). AEP cleaves synapsin at N82 in the brains of AD patients and generates the C-terminal synapsin Ⅰ (83-705) fragment. This fragment is abnormally distributed in neurons and induces synaptic dysfunction. Overexpression of AEP in the hippocampus of wild-type mice results in the production of the synapsin Ⅰ (83-705) fragment and induces synaptic dysfunction and cognitive deficits. Moreover, overexpression of the AEP-generated synapsin Ⅰ (83-705) fragment in the hippocampus of tau P301S transgenic mice and wild-type mice promotes synaptic dysfunction and cognitive deficits. These findings suggest a novel mechanism of synaptic dysfunction in AD.
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