ArticleAlzheimer's & dementia : the journal of the Alzheimer's Association2025
Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models.
Article in Alzheimer's & dementia : the journal of the Alzheimer's Association, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 2 papers.
What it found
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Who cites it
2 citing papers in PubMed.
- Effects of UMP, Choline, and Fish Oil on Synaptic Integrity and Motor Coordination in an Alzheimer's Disease Mouse Model.International journal of molecular sciences · 2026Article
- Direct evidence for dendritic spine compensation and regeneration in Alzheimer's disease models.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
Corrections and comments
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Authors and funding
7 authors.
Funding
Abstract
introductionDendritic spine loss in Alzheimer's disease (AD) strongly correlates with cognitive decline, whereas spine preservation is associated with cognitive resilience. Yet, whether and how neurons compensate for spine loss in AD remains largely unknown.
methodsWe developed a chromophore-assisted light inactivation (CALI) strategy to selectively eliminate dendritic spines to model this key feature of AD. Two-photon microscopy was used to monitor the structural plasticity of spines over time after spine elimination. Validation experiments were conducted in amyloid beta (Aβ)-driven models of synapse loss, including APP/PS1 mice and intracortical delivery of oligomeric Aβ.
resultsWe discovered that dendritic spine elimination-induced either artificially or in Aβ models-triggers a two-stage compensatory response: rapid enlargement of remaining spines followed by delayed spine regeneration. DISCUSSION: These findings provide direct evidence that neurons retain an intrinsic capacity to reverse early synaptic loss in AD, potentially contributing to cognitive resilience. HIGHLIGHTS: We developed a targeted optogenetic tool to selectively eliminate individual dendritic spines in live neurons, both in vitro and in vivo. We discovered a two-stage compensatory response to spine loss: rapid enlargement of surviving spines followed by delayed regeneration. We showed that the compensatory enlargement of dendritic spines depends on N-methyl-D-aspartate receptor activation and protein synthesis. We validated across multiple Alzheimer's disease models, demonstrating that similar compensatory plasticity occurs after amyloid beta oligomer-induced synapse loss. We postulate that synaptic resilience is an active neuronal program rather than a passive byproduct of pathology.
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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 Socratic graph.