ReviewMolecular brain2012
Alzheimer's disease Aβ assemblies mediating rapid disruption of synaptic plasticity and memory.
Review in Molecular brain, 2012. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 53 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.
Neither the registry nor the abstract names a trial number. If this is a trial report, that itself is worth knowing.
Who cites it
53 citing papers in PubMed, 97 citations in OpenAlex.
- Insulin Signaling in Alzheimer's Disease: Association with Brain Insulin Resistance.International journal of molecular sciences · 2026Review
- Understanding the Intersection Between Hormonal Dynamics and Brain Plasticity in Alzheimer's Disease: A Narrative Review for Implementing New Therapeutic Strategies.Health science reports · 2025Review
- Melatonin improves cognitive dysfunction and decreases gliosis in the streptozotocin-induced rat model of sporadic Alzheimer's disease.Frontiers in pharmacology · 2024Article
- Inhibition of ACAT as a Therapeutic Target for Alzheimer's Disease Is Independent of ApoE4 Lipidation.Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2023Article
- Soluble and insoluble protein aggregates, endoplasmic reticulum stress, and vascular dysfunction in Alzheimer's disease and cardiovascular diseases.GeroScience · 2023Review
- Synaptic Effects of Palmitoylethanolamide in Neurodegenerative Disorders.Biomolecules · 2022Review
- Bioactive human Alzheimer brain soluble Aβ: pathophysiology and therapeutic opportunities.Molecular psychiatry · 2022Review
- Vagus Nerve Stimulation as a Potential Therapy in Early Alzheimer's Disease: A Review.Frontiers in human neuroscience · 2022Review
- ACU193: An Immunotherapeutic Poised to Test the Amyloid β Oligomer Hypothesis of Alzheimer's Disease.Frontiers in neuroscience · 2022Review
- Insulin and Insulin Resistance in Alzheimer's Disease.International journal of molecular sciences · 2021Review
- Astrocytic MicroRNA in Ageing, Inflammation, and Neurodegenerative Disease.Frontiers in physiology · 2021Review
- A mechanistic hypothesis for the impairment of synaptic plasticity by soluble Aβ oligomers from Alzheimer's brain.Journal of neurochemistry · 2020Review
- Insulin Resistance at the Crossroad of Alzheimer Disease Pathology: A Review.Frontiers in endocrinology · 2020Review
- Hippocampal Deficits in Amyloid-β-Related Rodent Models of Alzheimer's Disease.Frontiers in neuroscience · 2020Review
- p110δ PI3-Kinase Inhibition Perturbs APP and TNFα Trafficking, Reduces Plaque Burden, Dampens Neuroinflammation, and Prevents Cognitive Decline in an Alzheimer's Disease Mouse Model.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2019Article
- Ion mobility spectrometry combined with multivariate statistical analysis: revealing the effects of a drug candidate for Alzheimer's disease on Aβ1-40 peptide early assembly.Analytical and bioanalytical chemistry · 2019Article
- The role of APOE in transgenic mouse models of AD.Neuroscience letters · 2019Review
- His6, His13, and His14 residues in Aβ 1-40 peptide significantly and specifically affect oligomeric equilibria.Scientific reports · 2019Article
- Effect of memantine combined with citalopram on cognition of BPSD and moderate Alzheimer's disease: A clinical trial.Experimental and therapeutic medicine · 2019Article
- Combined treatment with the phenolics (-)-epigallocatechin-3-gallate and ferulic acid improves cognition and reduces Alzheimer-like pathology in mice.The Journal of biological chemistry · 2019Article
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 1 institution in 2 countries.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Alzheimer's disease (AD) is characterized by episodic memory impairment that often precedes clinical diagnosis by many years. Probing the mechanisms of such impairment may provide much needed means of diagnosis and therapeutic intervention at an early, pre-dementia, stage. Prior to the onset of significant neurodegeneration, the structural and functional integrity of synapses in mnemonic circuitry is severely compromised in the presence of amyloidosis. This review examines recent evidence evaluating the role of amyloid-ß protein (Aβ) in causing rapid disruption of synaptic plasticity and memory impairment. We evaluate the relative importance of different sizes and conformations of Aβ, including monomer, oligomer, protofibril and fibril. We pay particular attention to recent controversies over the relevance to the pathophysiology of AD of different water soluble Aβ aggregates and the importance of cellular prion protein in mediating their effects. Current data are consistent with the view that both low-n oligomers and larger soluble assemblies present in AD brain, some of them via a direct interaction with cellular prion protein, cause synaptic memory failure. At the two extremes of aggregation, monomers and fibrils appear to act in vivo both as sources and sinks of certain metastable conformations of soluble aggregates that powerfully disrupt synaptic plasticity. The same principle appears to apply to other synaptotoxic amyloidogenic proteins including tau, α-synuclein and prion protein.
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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.