ReviewFrontiers in molecular neuroscience2017
AMPA Receptor Trafficking in Natural and Pathological Aging.
Review in Frontiers in molecular neuroscience, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 43 papers, 1 of them a synthesis that pooled it.
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Who cites it
43 citing papers in PubMed, 1 synthesis or guideline pooled it.
- Long Non-coding RNA: Insight Into Mechanisms of Alzheimer's Disease.Frontiers in molecular neuroscience · 2021Pooled it
- Age and sex-dependent alteration in AMPA receptor density in living human brain.European journal of nuclear medicine and molecular imaging · 2026Article
- Global hotspots and trends in AMPA receptor research (2000-2025): a bibliometric and visualization analysis.Naunyn-Schmiedeberg's archives of pharmacology · 2026Article
- The medial septum-hippocampus-lateral septum circuitry in spatial memory: linking healthy function to early Alzheimer's disease and translational opportunities.Translational neurodegeneration · 2025Review
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.Neurobiology of disease · 2025Article
- Amyloid-β-Driven Synaptic Deficits Are Mediated by Synaptic Removal of GluA3-Containing AMPA Receptors.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- AMPA receptor diffusional trapping machinery as an early therapeutic target in neurodegenerative and neuropsychiatric disorders.Translational neurodegeneration · 2025Review
- AMPA Receptors in Synaptic Plasticity, Memory Function, and Brain Diseases.Cellular and molecular neurobiology · 2025Review
- Loss of excitatory inputs and decreased tonic and evoked activity of locus coeruleus neurons in aged P301S mice.bioRxiv : the preprint server for biology · 2025Article
- Changes in the Properties of Ethanol-Sensitive Molecular Targets During Maturation and Aging.Advances in experimental medicine and biology · 2025Review
- A small molecule p38α MAPK inhibitor, MW150, attenuates behavioral deficits and neuronal dysfunction in a mouse model of mixed amyloid and vascular pathologies.Brain, behavior, & immunity - health · 2024Article
- A TrkB and TrkC partial agonist restores deficits in synaptic function and promotes activity-dependent synaptic and microglial transcriptomic changes in a late-stage Alzheimer's mouse model.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2024Article
- Familial Alzheimer's Disease Neurons Bearing Mutations inLife (Basel, Switzerland) · 2024Article
- Article
- Aging impairs recovery from stress-induced depression in male rats possibly by alteration of microRNA-101 expression and Rac1/RhoA pathway in the prefrontal cortex.Biogerontology · 2023Article
- Review
- Tauopathy and alcohol consumption interact to alter locus coeruleus excitatory transmission and excitability in male and female mice.Alcohol (Fayetteville, N.Y.) · 2023Article
- Aging in nucleus accumbens and its impact on alcohol use disorders.Alcohol (Fayetteville, N.Y.) · 2023Review
- Neurobiological Mechanisms of Cognitive Decline Correlated with Brain Aging.Advances in experimental medicine and biology · 2023Article
- Parkinson's disease, epilepsy, and amyotrophic lateral sclerosis-emerging role of AMPA and kainate subtypes of ionotropic glutamate receptors.Frontiers in cell and developmental biology · 2023Review
Corrections and comments
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1 author.
Funding
Abstract
α-amino-3-hydroxy-5-methyl-4-isoxazolepropionic acid receptors (AMPARs) enable most excitatory transmission in the brain and are crucial for mediating basal synaptic strength and plasticity. Because of the importance of their function, AMPAR dynamics, activity and subunit composition undergo a tight regulation which begins as early as prenatal development and continues through adulthood. Accumulating evidence suggests that the precise regulatory mechanisms involved in orchestrating AMPAR trafficking are challenged in the aging brain. In turn dysregulation of AMPARs can be linked to most neurological and neurodegenerative disorders. Understanding the mechanisms that govern AMPAR signaling during natural and pathological cognitive decline will guide the efforts to develop most effective ways to tackle neurodegenerative diseases which are one of the primary burdens afflicting an increasingly aging population. In this review, I provide a brief overview of the molecular mechanisms involved in AMPAR trafficking highlighting what is currently known about how these processes change with age and disease. As a particularly well-studied example of AMPAR dysfunction in pathological aging I focus in Alzheimer's disease (AD) with special emphasis in how the production of neurofibrillary tangles (NFTs) and amyloid-β plaques may contribute to disruption in AMPAR function.
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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.