ReviewNeural plasticity2016
Emerging Link between Alzheimer's Disease and Homeostatic Synaptic Plasticity.
Review in Neural plasticity, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 56 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
56 citing papers in PubMed, 92 citations in OpenAlex.
- Functional and structural characterization of dendritic spine pathology in a mouse model of tauopathy.iScience · 2026Article
- Temporal and Cell-Specific Regulation of Synaptic Homeostasis by the Chromatin Remodeler Chd1.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Effects of Wheat Malt Extract on Molecular and Behavioral Markers in Aged APP/PS1 and Wild-Type Mice.International journal of molecular sciences · 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
- Regulation of presynaptic homeostatic plasticity by glial signalling in Alzheimer's disease.The Journal of physiology · 2025Review
- The Role and Pathogenesis of Tau Protein in Alzheimer's Disease.Biomolecules · 2025Review
- ADAR2-mediated Q/R editing of GluA2 in homeostatic synaptic plasticity.Science signaling · 2025Article
- Targeting Tiam1 Enhances Hippocampal-Dependent Learning and Memory in the Adult Brain and Promotes NMDA Receptor-Mediated Synaptic Plasticity and Function.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2025Article
- Homeostatic plasticity in patients with disorders of consciousness detected by combined stimulation: a study protocol.Frontiers in neurology · 2025Article
- SIK1 Downregulates Synaptic AMPA Receptors and Contributes to Cognitive Defects in Alzheimer's Disease.Molecular neurobiology · 2024Article
- ProSAAS is preferentially up-regulated during homeostatic scaling and reduces amyloid plaque burden in the 5xFAD mouse hippocampus.Journal of neurochemistry · 2024Article
- Synapses tagged, memories kept: synaptic tagging and capture hypothesis in brain health and disease.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Review
- ProSAAS is Preferentially Secreted from Neurons During Homeostatic Scaling and Reduces Amyloid Plaque Size in the 5xFAD Mouse Hippocampus.bioRxiv : the preprint server for biology · 2024Article
- Amyloid Pathology Impairs Experience-Dependent Inhibitory Synaptic Plasticity.The Journal of neuroscience : the official journal of the Society for Neuroscience · 2024Article
- Non-rapid eye movement sleep slow-wave activity features are associated with amyloid accumulation in older adults with obstructive sleep apnoea.Brain communications · 2024Article
- Amyloid pathology impairs experience-dependent inhibitory synaptic plasticity.bioRxiv : the preprint server for biology · 2023Article
- Article
- Role of α2δ-3 in regulating calcium channel localization at presynaptic active zones during homeostatic plasticity.Frontiers in molecular neuroscience · 2023Article
- A glutamate receptor C-tail recruits CaMKII to suppress retrograde homeostatic signaling.Nature communications · 2022Article
- Paclitaxel induces cognitive impairment via necroptosis, decreased synaptic plasticity and M1 polarisation of microglia.Pharmaceutical biology · 2022Article
Corrections and comments
PubMed lists nothing against this paper. Absence here is not a guarantee, only a check that was made.
Authors and funding
2 authors at 1 institution in 1 country.
Funding
Abstract
Alzheimer's disease (AD) is an irreversible brain disorder characterized by progressive cognitive decline and neurodegeneration of brain regions that are crucial for learning and memory. Although intracellular neurofibrillary tangles and extracellular senile plaques, composed of insoluble amyloid-β (Aβ) peptides, have been the hallmarks of postmortem AD brains, memory impairment in early AD correlates better with pathological accumulation of soluble Aβ oligomers and persistent weakening of excitatory synaptic strength, which is demonstrated by inhibition of long-term potentiation, enhancement of long-term depression, and loss of synapses. However, current, approved interventions aiming to reduce Aβ levels have failed to retard disease progression; this has led to a pressing need to identify and target alternative pathogenic mechanisms of AD. Recently, it has been suggested that the disruption of Hebbian synaptic plasticity in AD is due to aberrant metaplasticity, which is a form of homeostatic plasticity that tunes the magnitude and direction of future synaptic plasticity based on previous neuronal or synaptic activity. This review examines emerging evidence for aberrant metaplasticity in AD. Putative mechanisms underlying aberrant metaplasticity in AD will also be discussed. We hope this review inspires future studies to test the extent to which these mechanisms contribute to the etiology of AD and offer therapeutic targets.
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.