ArticleCell reports2021
PSD-95 protects synapses from β-amyloid.
Article in Cell reports, 2021. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 93 papers, 1 of them a synthesis that pooled it.
What it found
Each row is one number read from the abstract, on the scale the paper reported it, with its interval. Left of the dashed line favours the treatment, right favours the comparator. Under each row is the sentence it came from. New to these charts? A ten-minute tutorial.
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
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
93 citing papers in PubMed, 1 synthesis or guideline pooled it, 125 citations in OpenAlex.
- Effect of exercise on cognitive function and synaptic plasticity in Alzheimer's disease models: A systematic review and meta-analysis.Frontiers in aging neuroscience · 2022Pooled it
- The role of protein palmitoylation in disease pathogenesis and therapeutic innovation.Annals of medicine · 2026Review
- Emerging roles of α/β hydrolase domain (ABHD) proteins in S-palmitoylation modification: molecular mechanisms, structural features, and pathological implications.Cellular & molecular biology letters · 2026Review
- Sleep Deprivation Induces Glial Dysfunction, Synaptic Loss, Metabolic Imbalance, and Cognitive Impairment in 12-Month-Old Mice: Protective Effects of D30.CNS neuroscience & therapeutics · 2026Article
- Article
- Genomic landscape of rare variants in a Chinese autism cohort and discovery of novel risk genes.Molecular psychiatry · 2026Article
- PDE4A knockdown rescues alcohol-induced cognitive impairment and synaptic dysfunction via the cAMP/PKA/CREB pathway.The international journal of neuropsychopharmacology · 2026Article
- HDAC11 as a potential therapeutic target for Alzheimer's disease.Drug discovery today · 2026Review
- Article
- Patient cerebral organoids capture Alzheimer's disease proteomic biomarkers and drug targets.bioRxiv : the preprint server for biology · 2026Article
- ESCRT-0 regulates AMPA receptor currents and CabioRxiv : the preprint server for biology · 2026Article
- High intensity 40 Hz flicker improves amyloid pathology and cognition with autophagy in 3xTg mice.iScience · 2026Article
- ProteinJournal of pharmaceutical analysis · 2026Review
- Pharmacological insights into deoxyelephantopin: a multifunctional sesquiterpene with therapeutic promise in cancer and neurodegenerative disorders.Molecular biology reports · 2026Review
- Article
- Emerging Roles of GluN3B NMDA Receptor Subunit in the Central Nervous System.Neuroscience bulletin · 2026Review
- CB2R-mediated GPX4 stabilization: a new avenue for treating cognitive impairment in elderly migraine patients.The journal of headache and pain · 2026Article
- Sex-dependent rescue of memory and synaptic deficits in AD model mice by increasing PSD-95 palmitoylation.Communications biology · 2026Article
- Bioinformatics Analysis of ZDHHC-protein Acyltransferase for Predicting the Rupture of Aneurysmal Subarachnoid Hemorrhage.Current neurovascular research · 2026Article
- Fucoxanthin attenuates carbonyl stress and neuroinflammation by modulating MGO/RAGE/NF-κB axis in Aβ-induced models.Frontiers in pharmacology · 2026Article
33 more citing papers are in PubMed but not listed here.
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
7 authors at 2 institutions in 2 countries.
Funding
Abstract
Beta-amyloid (Aβ) depresses excitatory synapses by a poorly understood mechanism requiring NMDA receptor (NMDAR) function. Here, we show that increased PSD-95, a major synaptic scaffolding molecule, blocks the effects of Aβ on synapses. The protective effect persists in tissue lacking the AMPA receptor subunit GluA1, which prevents the confounding synaptic potentiation by increased PSD-95. Aβ modifies the conformation of the NMDAR C-terminal domain (CTD) and its interaction with protein phosphatase 1 (PP1), producing synaptic weakening. Higher endogenous levels or overexpression of PSD-95 block Aβ-induced effects on the NMDAR CTD conformation, its interaction with PP1, and synaptic weakening. Our results indicate that increased PSD-95 protects synapses from Aβ toxicity, suggesting that low levels of synaptic PSD-95 may be a molecular sign indicating synapse vulnerability to Aβ. Importantly, pharmacological inhibition of its depalmitoylation increases PSD-95 at synapses and rescues deficits caused by Aβ, possibly opening a therapeutic avenue against Alzheimer's disease.
Indexed as
Identifiers
What OpenQuestion holds
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.