ArticleNature communications2018
Overexpression of endophilin A1 exacerbates synaptic alterations in a mouse model of Alzheimer's disease.
Article in Nature communications, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 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.
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Who cites it
31 citing papers in PubMed, 58 citations in OpenAlex.
- Molecular Signaling Pathways in Depression and Neuroinflammation: Focus on New Pathophysiological Proteins and Therapeutic Compounds.Antioxidants (Basel, Switzerland) · 2026Review
- Programmed cell death: a promising management for Alzheimer's disease.Apoptosis : an international journal on programmed cell death · 2026Review
- Mitochondrial oxidative stress promotes the accumulation of advanced glycation end products.PloS one · 2026Article
- Common themes in evoked ion channel translocation in neuroplastic and homeostatic plasticity.Frontiers in pharmacology · 2026Review
- PINK1-dependent NFKB signaling contributes to amyloid pathology in Alzheimer disease.Autophagy · 2025Article
- Article
- Bending the boundaries: the many facets of endophilin-As from membrane dynamics to disease.Cellular and molecular life sciences : CMLS · 2025Review
- Neurons Specialize in Presynaptic Autophagy: A Perspective to Ameliorate Neurodegeneration.Molecular neurobiology · 2025Review
- Research progress on plant-derived natural compounds regulating the MAPK signaling pathway for the prevention and therapy of Alzheimer's disease.Frontiers in pharmacology · 2025Review
- CD2AP deficiency aggravates Alzheimer's disease phenotypes and pathology through p38 MAPK activation.Translational neurodegeneration · 2024Article
- Glucocorticoid stress hormones stimulate vesicle-free Tau secretion and spreading in the brain.Cell death & disease · 2024Article
- Identification of the Shared Gene Signatures Between Alzheimer's Disease and Diabetes-Associated Cognitive Dysfunction by Bioinformatics Analysis Combined with Biological Experiment.Journal of Alzheimer's disease : JAD · 2024Article
- Kai-Xin-San protects against mitochondrial dysfunction in Alzheimer's disease through SIRT3/NLRP3 pathway.Chinese medicine · 2023Article
- The Role of Endophilin A1 in Lipopolysaccharide-Induced Parkinson's Disease Model Mice.Journal of Parkinson's disease · 2023Article
- Small molecules targeting endocytic uptake and recycling pathways.Frontiers in cell and developmental biology · 2023Review
- Biology of endophilin and it's role in disease.Frontiers in immunology · 2023Review
- Local regulation of extracellular vesicle traffic by the synaptic endocytic machinery.The Journal of cell biology · 2022Article
- Inhibiting amyloid beta (1-42) peptide-induced mitochondrial dysfunction prevents the degradation of synaptic proteins in the entorhinal cortex.Frontiers in aging neuroscience · 2022Article
- Mitochondrial-Respiration-Improving Effects of Three Different Gardeniae Fructus Preparations and Their Components.ACS omega · 2021Article
- Disentangling Mitochondria in Alzheimer's Disease.International journal of molecular sciences · 2021Review
Corrections and comments
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Authors and funding
13 authors at 5 institutions in 4 countries.
Funding
Abstract
Endophilin A1 (EP) is a protein enriched in synaptic terminals that has been linked to Alzheimer's disease (AD). Previous in vitro studies have shown that EP can bind to a variety of proteins, which elicit changes in synaptic transmission of neurotransmitters and spine formation. Additionally, we previously showed that EP protein levels are elevated in AD patients and AD transgenic animal models. Here, we establish the in vivo consequences of upregulation of EP expression in amyloid-β peptide (Aβ)-rich environments, leading to changes in both long-term potentiation and learning and memory of transgenic animals. Specifically, increasing EP augmented cerebral Aβ accumulation. EP-mediated signal transduction via reactive oxygen species (ROS)/p38 mitogen-activated protein (MAP) kinase contributes to Aβ-induced mitochondrial dysfunction, synaptic injury, and cognitive decline, which could be rescued by blocking either ROS or p38 MAP kinase activity.
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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.