ArticleMolecular medicine reports2019
Endophilin 1 knockdown prevents synaptic dysfunction induced by oligomeric amyloid β.
Article in Molecular medicine reports, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 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.
The trial behind it
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Who cites it
7 citing papers in PubMed, 7 citations in OpenAlex.
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- STED Imaging of Vesicular Endocytosis in the Synapse.Neuroscience bulletin · 2024Article
- The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson's Disease Model Mice.Journal of Parkinson's disease · 2023Article
- Biology of endophilin and it's role in disease.Frontiers in immunology · 2023Review
- Molecular Insight Into the Therapeutic Potential of Long Non-coding RNA-Associated Competing Endogenous RNA Axes in Alzheimer's Disease: A Systematic Scoping Review.Frontiers in aging neuroscience · 2021Article
- Competing Endogenous RNA Networks as Biomarkers in Neurodegenerative Diseases.International journal of molecular sciences · 2020Review
- Molecular mechanism of Fast Endophilin-Mediated Endocytosis.The Biochemical journal · 2020Review
Corrections and comments
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Authors and funding
8 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Amyloid β (Aβ) has been reported to have an important role in the cognitive deficits of Alzheimer's disease (AD), as oligomeric Aβ promotes synaptic dysfunction and triggers neuronal death. Recent evidence has associated an endocytosis protein, endophilin 1, with AD, as endophilin 1 levels have been reported to be markedly increased in the AD brain. The increase in endophilin 1 levels in neurons is associated with an increase in the activation of the stress kinase JNK, with subsequent neuronal death. In the present study, whole‑cell patch‑clamp recording demonstrated that oligomeric Aβ caused synaptic dysfunction and western blotting revealed that endophilin 1 was highly expressed prior to neuronal death of cultured hippocampal neurons. Furthermore, RNA interference and electrophysiological recording techniques in cultured hippocampal neurons demonstrated that knockdown of endophilin 1 prevented synaptic dysfunction induced by Aβ. Thus, a potential role for endophilin 1 in Aβ‑induced postsynaptic dysfunction has been identified, indicating a possible direction for the prevention of postsynaptic dysfunction in cognitive impairment and suggesting that endophilin may be a potential target for the clinical treatment of 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.