ArticleAlzheimer's & dementia (New York, N. Y.)2019
Amyloid-β oligomers suppress subunit-specific glutamate receptor increase during LTP.
Article in Alzheimer's & dementia (New York, N. Y.), 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 12 papers.
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Who cites it
12 citing papers in PubMed, 18 citations in OpenAlex.
- Toxic mechanisms of amyloid oligomers and therapeutic strategies.Protein science : a publication of the Protein Society · 2026Review
- Review
- Article
- Decanoic Acid Rescues Differences in AMPA-Mediated Calcium Rises in Hippocampal CA1 Astrocytes and Neurons in the 5xFAD Mouse Model of Alzheimer's Disease.Biomolecules · 2023Article
- Potential mechanisms underlying lithium treatment for Alzheimer's disease and COVID-19.European review for medical and pharmacological sciences · 2022Review
- Positron Emission Tomography in Animal Models of Alzheimer's Disease Amyloidosis: Translational Implications.Pharmaceuticals (Basel, Switzerland) · 2021Review
- Allosteric modulation of AMPA receptors counteracts Tau-related excitotoxic synaptic signaling and memory deficits in stress- and Aβ-evoked hippocampal pathology.Molecular psychiatry · 2021Article
- Emerging role of AMPA receptor subunit GluA1 in synaptic plasticity: Implications for Alzheimer's disease.Cell proliferation · 2021Review
- The Role of Non-coding RNAs in Alzheimer's Disease: From Regulated Mechanism to Therapeutic Targets and Diagnostic Biomarkers.Frontiers in aging neuroscience · 2021Review
- Aberrant Synaptic PTEN in Symptomatic Alzheimer's Patients May Link Synaptic Depression to Network Failure.Frontiers in synaptic neuroscience · 2021Article
- Guanosine Neuroprotection of Presynaptic Mitochondrial Calcium Homeostasis in a Mouse Study with Amyloid-β Oligomers.Molecular neurobiology · 2020Article
- Acetylation of AMPA Receptors Regulates Receptor Trafficking and Rescues Memory Deficits in Alzheimer's Disease.iScience · 2020Article
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Authors and funding
3 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
introductionAmyloid-β oligomers (AβOs) are assumed to impair the ability of learning and memory by suppressing the induction of synaptic plasticity, such as long-term potentiation (LTP) in the early stage of Alzheimer's disease. However, the direct molecular mechanism of how AβOs affect excitatory synaptic plasticity remains to be elucidated.
methodsIn order to study the effects of AβOs on LTP-associated changes of AMPA (alpha-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid)-type glutamate receptor (AMPAR) movement, we performed live-cell imaging of fluorescently labeled AMPAR subunit GluA1 or GluA2 with total internal reflection fluorescence microscopy.
resultsIncubation of cultured hippocampal neurons with AβOs for 1-2 days inhibited the increase in GluA1 number and GluA1 exocytosis frequency in both postsynaptic and extrasynaptic membranes during LTP. In contrast, AβOs did not inhibit the increase in GluA2 number or exocytosis frequency. DISCUSSION: These results suggest that AβOs primarily inhibit the increase in the number of GluA1 homomers and suppress hippocampal LTP expression.
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