ReviewNeurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology2016
Dysfunction of NMDA receptors in Alzheimer's disease.
Review in Neurological sciences : official journal of the Italian Neurological Society and of the Italian Society of Clinical Neurophysiology, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 126 papers.
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
126 citing papers in PubMed, 264 citations in OpenAlex.
- Targeting neuroplasticity in old brain: restoring synapse with cognitive strategies.Biogerontology · 2026Review
- GluN2A-mediated currents and calcium signal in human iPSC-derived neurons.Scientific reports · 2026Article
- Effects of Continuous Theta Burst Stimulation on Behavior and NMDA Receptor Subunits in the Trimethyltin-Induced Alzheimer's-like Disease Model.Biomedicines · 2026Article
- Design, Synthesis and Anti-Alzheimer's Activity of Some Hybrid Molecule of Oxymatrine Through TGF-β.Current topics in medicinal chemistry · 2026Article
- Transcranial magnetic stimulation from healthy brain aging to Alzheimer's disease: a review on mechanisms, therapeutic potential, and future clinical directions.Frontiers in aging neuroscience · 2026Review
- Tat-NR2B9c prevent cognitive dysfunction in mice modeling Alzheimer's Disease induced by AβIBRO neuroscience reports · 2025Article
- Article
- Decoding natural products for neuroprotection: Pathway networks and structural insights for drug development.Chinese herbal medicines · 2025Review
- Targeting the serotonergic system in the treatment of neurodegenerative diseases-emerging therapies and unmet challenges.Pharmacological reviews · 2025Review
- A phosphoserine phosphatase variant present in the brain of Alzheimer's disease patients favors nuclear mistargeting.The FEBS journal · 2025Article
- Alterations of NMDAR Subunits in the Cerebrospinal Fluid Across Neurodegenerative and Immunological Disorders.Journal of neurochemistry · 2025Article
- Advancing Care in Alzheimer's Disease: Current Treatments and Their Impact on Quality of Life.Cureus · 2025Review
- Natural aminosterols inhibit NMDA receptors with low nanomolar potency.The FEBS journal · 2025Article
- Role of Ion Channels in Alzheimer's Disease Pathophysiology.The Journal of membrane biology · 2025Review
- Dysregulated Neurotransmission and the Role of Viruses in Alzheimer's Disease.ACS chemical neuroscience · 2025Review
- Comprehensive investigation of multiple targets in the development of newer drugs for the Alzheimer's disease.Acta pharmaceutica Sinica. B · 2025Review
- Review
- Ketamine does not rescue plaque load or gap detection in the 5XFAD mouse model of Alzheimer's disease.Frontiers in aging neuroscience · 2025Article
- Article
- Hippocampal Synaptic Plasticity: Integrating Memory and Anxiety Impairments in the Early Stages of Alzheimer's Disease.Current topics in behavioral neurosciences · 2025Review
66 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
4 authors at 3 institutions in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
N-methyl-D-aspartate receptors (NMDARs) play a pivotal role in the synaptic transmission and synaptic plasticity thought to underlie learning and memory. NMDARs activation has been recently implicated in Alzheimer's disease (AD) related to synaptic dysfunction. Synaptic NMDARs are neuroprotective, whereas overactivation of NMDARs located outside of the synapse cause loss of mitochondrial membrane potential and cell death. NMDARs dysfunction in the glutamatergic tripartite synapse, comprising presynaptic and postsynaptic neurons and glial cells, is directly involved in AD. This review discusses that both beta-amyloid (Aβ) and tau perturb synaptic functioning of the tripartite synapse, including alterations in glutamate release, astrocytic uptake, and receptor signaling. Particular emphasis is given to the role of NMDARs as a possible convergence point for Aβ and tau toxicity and possible reversible stages of the AD through preventive and/or disease-modifying therapeutic strategies.
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.