ReviewEBioMedicine2025
Synapse vulnerability and resilience underlying Alzheimer's disease.
Review in EBioMedicine, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 21 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
21 citing papers in PubMed.
- Local autophagy impairment triggers brain-wide presynaptic remodeling and resilience.The EMBO journal · 2026Article
- The UNC13A cryptic exon associates with cognitive impairment in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Retinal proteome changes mirror brain pathology and reveal synaptic and cytoskeletal dysfunction in Alzheimer's disease.Acta neuropathologica · 2026Article
- Dorsolateral Prefrontal Cortex Circuitry at the Intersection of Cognition and Disease.Biological psychiatry · 2026Review
- Article
- Comprehensive single-cell transcriptomic atlas of microglia in Alzheimer's disease mouse models.Molecular psychiatry · 2026Article
- Distinct regional patterns of synaptic vulnerability across hippocampal and parahippocampal subregions in Alzheimer's disease.Brain pathology (Zurich, Switzerland) · 2026Article
- AETA peptide contributes to Alzheimer's disease signature of synapse dysfunction.Acta neuropathologica · 2026Article
- 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
- The Amyloid Plaque Proteomes of Alzheimer's Disease and Mild Cognitive Impairment.Research square · 2026Article
- Small molecule modulation of the p75 neurotrophin receptor promotes dendritic spine resilience to pathogenic tau species and reduces their accumulation.Acta neuropathologica communications · 2026Article
- Selective vulnerability of human synapses to soluble tau oligomers.Journal of Alzheimer's disease : JAD · 2026Article
- Challenges and Opportunities of Drug Delivery for Treatment of Alzheimer's Disease.AAPS PharmSciTech · 2026Review
- Progressive changes in synapses and glial cells inBrain communications · 2026Article
- Synaptic micromechanics and brain softening as a mechanobiological hypothesis for Alzheimer's disease.Frontiers in neuroscience · 2026Article
- Alismatis Rhizoma prevents AβO-induced neuronal cell death and synaptic loss in Alzheimer's disease models.Frontiers in pharmacology · 2026Article
- Associations of cerebrospinal fluid measures of synaptic function with white matter microstructure and cognition in older adults.Frontiers in aging neuroscience · 2026Article
- Neuroinflammatory stress preferentially impacts synaptic MAPK signaling and mitochondria in excitatory neurons.Molecular neurodegeneration advances · 2026Article
- Noninvasive Brain Stimulation Protects Cognitive Impairment in i.c.v. STZ-Injected Rats: Role of Adult Neurogenesis.The European journal of neuroscience · 2025Article
- Synaptic loss pattern is constrained by brain connectome and modulated by phosphorylated tau in Alzheimer's disease.Nature communications · 2025Article
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.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Synapse preservation is key for healthy cognitive ageing, and synapse loss represents a critical anatomical basis of cognitive dysfunction in Alzheimer's disease (AD), predicting dementia onset, severity, and progression. Synapse loss is viewed as a primary pathologic event, preceding neuronal loss and brain atrophy in AD. Synapses may, therefore, represent one of the earliest and clinically most meaningful targets of the neuropathologic processes driving AD dementia. The synapse loss in AD is highly selective and targets particularly vulnerable synapses while leaving others, termed resilient, largely unaffected. Yet, the anatomic and molecular hallmarks of the vulnerable and resilient synapse populations and their association with AD neuropathologic changes (e.g. amyloid-β plaques and tau tangles) and memory dysfunction remain poorly understood. Characterising the selectively vulnerable and resilient synapses in AD may be key to understanding the mechanisms of cognitive preservation versus loss and enable the development of robust biomarkers and disease-modifying therapies for dementia.
Indexed as
Identifiers
What Socratic 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 Socratic graph.