ReviewNeuromolecular medicine2010
Alzheimer's disease amyloid beta-protein and synaptic function.
Review in Neuromolecular medicine, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 73 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.
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.
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Who cites it
73 citing papers in PubMed, 141 citations in OpenAlex.
- Oxiracetam Improves Cognitive Disorder in AD by Modulating AMPAR Subunits GluA1/GluA2 Kinetics.Cell biochemistry and biophysics · 2026Article
- PP2A methylesterase, PME-1, and PP2A methyltransferase, LCMT-1, control sensitivity to impairments caused by injury-related oligomeric tau.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Divergent disruptive effects of soluble recombinant tau assemblies on synaptic plasticity in vivo.Molecular brain · 2025Article
- Teucrium Polium ameliorates amyloid β-induced brain network disorders in rats: electrophysiological and behavioral studies.BMC complementary medicine and therapies · 2025Article
- Development of Neurodegenerative Disease Diagnosis and Monitoring from Traditional to Digital Biomarkers.Biosensors · 2025Review
- Navβ2 Intracellular Fragments Contribute to Aβ1-42-Induced Cognitive Impairment and Synaptic Deficit Through Transcriptional Suppression of BDNF.Molecular neurobiology · 2025Article
- A combination of ΔNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2024Article
- Patient-derived tau and amyloid-β facilitate long-term depressionBrain communications · 2024Article
- mGluR-dependent plasticity in rodent models of Alzheimer's disease.Frontiers in synaptic neuroscience · 2023Article
- Early and late chaperone intervention therapy boosts XBP1s and ADAM10, restores proteostasis, and rescues learning in Alzheimer's Disease mice.Aging biology · 2023Article
- Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities.Molecular psychiatry · 2022Review
- Modulation of Amyloid β-Induced Microglia Activation and Neuronal Cell Death by Curcumin and Analogues.International journal of molecular sciences · 2022Article
- Differential vulnerability of hippocampal CA3-CA1 synapses to Aβ.Acta neuropathologica communications · 2022Article
- ACU193: An Immunotherapeutic Poised to Test the Amyloid β Oligomer Hypothesis of Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Roles and Mechanisms of the Protein Quality Control System in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- The Density of Group I mGluInternational journal of molecular sciences · 2021Article
- Developmental synaptic regulator, TWEAK/Fn14 signaling, is a determinant of synaptic function in models of stroke and neurodegeneration.Proceedings of the National Academy of Sciences of the United States of America · 2021Article
- Downregulation of autophagy by 12/15Lipoxygenase worsens the phenotype of an Alzheimer's disease mouse model with plaques, tangles, and memory impairments.Molecular psychiatry · 2021Article
- Alzheimer's Disease and Protein Kinases.Advances in experimental medicine and biology · 2021Article
- Physical Stress Induced Reduction of Proliferating Cells and Differentiated Neuroblasts Is Ameliorated by FermentedMarine drugs · 2020Article
13 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
6 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized neuropathologically by the deposition of different forms of amyloid beta-protein (A beta) including variable amounts of soluble species that correlate with severity of dementia. The extent of synaptic loss in the brain provides the best morphological correlate of cognitive impairment in clinical AD. Animal research on the pathophysiology of AD has therefore focussed on how soluble A beta disrupts synaptic mechanisms in vulnerable brain regions such as the hippocampus. Synaptic plasticity in the form of persistent activity-dependent increases or decreases in synaptic strength provide a neurophysiological substrate for hippocampal-dependent learning and memory. Acute treatment with human-derived or chemically prepared soluble A beta that contains certain oligomeric assemblies, potently and selectively disrupts synaptic plasticity causing inhibition of long-term potentiation (LTP) and enhancement of long-term depression (LTD) of glutamatergic transmission. Over time these and related actions of A beta have been implicated in reducing synaptic integrity. This review addresses the involvement of neurotransmitter intercellular signaling in mediating or modulating the synaptic plasticity disrupting actions of soluble A beta, with particular emphasis on the different roles of glutamatergic and cholinergic mechanisms. There is growing evidence to support the view that NMDA and possibly nicotinic receptors are critically involved in mediating the disruptive effect of A beta and that targeting muscarinic receptors can indirectly modulate A beta's actions. Such studies should help inform ongoing and future clinical trials of drugs acting through the glutamatergic and cholinergic systems.
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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.