ReviewThe Journal of neuroscience : the official journal of the Society for Neuroscience2023
Synaptic Compensatory Plasticity in Alzheimer's Disease.
Review in The Journal of neuroscience : the official journal of the Society for Neuroscience, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 31 papers.
What it found
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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
31 citing papers in PubMed.
- An aging-sensitive secreted phospholipase confers neuroprotection and cognitive resilience.Nature neuroscience · 2026Article
- Ultrastructural Evidence of Altered Dendritic Morphology in the Prefrontal Cortex of Alzheimer's Model Rats.Neuroscience bulletin · 2026Article
- Emerging diagnostic biomarkers and therapeutic targets in Alzheimer's disease.Inflammopharmacology · 2026Review
- Article
- Review
- Divergent white matter metabolic signature patterns indicate impending cognitive decline in aging and dementia.Nature communications · 2026Article
- Neuronal Extracellular Vesicles Carrying APOE Downregulate Filament Actin Polymerization Signaling to Inhibit Synapse Formation in Alzheimer's Disease.Journal of extracellular vesicles · 2026Article
- Utilisation of Machine Learning Approaches Improves RNA-Seq Transcriptome Analyses in Alzheimer's Disease Brain.Journal of molecular neuroscience : MN · 2026Article
- TNEA Regulates Hippocampal Oscillation by Improving Inhibitory Synaptic Plasticity to Ameliorates Cognitive Impairment in Alzheimer's Disease.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Article
- Midbrain extracellular matrix and microglia are associated with cognition in aging mice.Nature communications · 2025Article
- The Impact of Insulin Resistance on Grey Matter Changes Along the Alzheimer's Disease Continuum Insulin Resistance and Grey Matter in AD.medRxiv : the preprint server for health sciences · 2025Article
- Integrating imaging and omics for enhanced subtyping of mild cognitive impairment associated with Alzheimer's disease.Journal of translational medicine · 2025Article
- Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Frequency and duration of sensory flicker control transcriptional profiles in 5xFAD mice.APL bioengineering · 2025Article
- Boosting angiotensin-converting enzyme (ACE) in microglia protects against Alzheimer's disease in 5xFAD mice.Nature aging · 2025Article
- Time-Frequency Domain Analysis of Quantitative Electroencephalography as a Biomarker for Dementia.Diagnostics (Basel, Switzerland) · 2025Review
- Study on the protective effects and mechanisms of eleutherococcus senticosus on korsakoff syndrome.Frontiers in neuroscience · 2025Review
- Resource-dependent heterosynaptic spike-timing-dependent plasticity in recurrent networks with and without synaptic degeneration.Frontiers in computational neuroscience · 2025Article
- Enhanced prefrontal nicotinic signaling as evidence of active compensation in Alzheimer's disease models.Translational neurodegeneration · 2024Article
Corrections and comments
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Authors and funding
3 authors.
Funding
Abstract
The loss of excitatory synapses is known to underlie the cognitive deficits in Alzheimer's disease (AD). Although much is known about the mechanisms underlying synaptic loss in AD, how neurons compensate for this loss and whether this provides cognitive benefits remain almost completely unexplored. In this review, we describe two potential compensatory mechanisms implemented following synaptic loss: the enlargement of the surviving neighboring synapses and the regeneration of synapses. Because dendritic spines, the postsynaptic site of excitatory synapses, are easily visualized using light microscopy, we focus on a range of microscopy approaches to monitor synaptic loss and compensation. Here, we stress the importance of longitudinal dendritic spine imaging, as opposed to fixed-tissue imaging, to gain insights into the temporal dynamics of dendritic spine compensation. We believe that understanding the molecular mechanisms behind these and other forms of synaptic compensation and regeneration will be critical for the development of therapeutics aiming at delaying the onset of cognitive deficits in AD.
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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.