ReviewBrain communications2022
Emerging insights into synapse dysregulation in Alzheimer's disease.
Review in Brain communications, 2022. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers, 3 of them syntheses that pooled it.
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
30 citing papers in PubMed, 3 syntheses or guidelines pooled it, 42 citations in OpenAlex.
- Synaptic biomarkers in Alzheimer's disease dementia and mild cognitive impairment: A systematic review and meta-analysis.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Pooled it
- Functional and effective EEG connectivity patterns in Alzheimer's disease and mild cognitive impairment: a systematic review.Frontiers in aging neuroscience · 2025Pooled it
- A Meta-Analysis on Presynaptic Changes in Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2024Pooled it
- Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- The UNC13A cryptic exon associates with cognitive impairment in Alzheimer's disease.Alzheimer's research & therapy · 2026Article
- Amyloid-beta induces distinct forms of cell death in different neuronal populations.Cell death and differentiation · 2026Article
- Omega-3 Fatty Acids and Alzheimer's Disease: Toward a New Understanding of Neuroprotective Mechanisms and Intervention Strategies.Marine drugs · 2026Review
- miR-125b Mediates Tau-induced Mitochondrial Dysfunction in a Cellular Model of Alzheimer's Disease.Molecular neurobiology · 2026Article
- Selective vulnerability of human synapses to soluble tau oligomers.Journal of Alzheimer's disease : JAD · 2026Article
- Low concentrations of amyloid-beta oligomers induce synaptogenesis characteristic for mild cognitive impairment and alter the de novo proteome.Translational psychiatry · 2026Article
- Cognitive resilience in preclinical Alzheimer's disease: Higher NPTX2 and VGF levels are associated with reduced cognitive decline.Neurobiology of aging · 2025Article
- Evolutionary sex bias in cognitive response to new environmental risk factor - PM2.5.Biology of sex differences · 2025Review
- Cerebrospinal fluid neuronal pentraxin levels are associated with tau pathology via microglia-astrocyte signaling in alzheimer's disease.Journal of neuroinflammation · 2025Article
- Insulin resistance and cognitive decline: the metabolic mechanisms linking type 2 diabetes to Alzheimer's disease.Diabetology international · 2025Review
- Comprehensive characterization of the RNA editing landscape in the human aging brains with Alzheimer's disease.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2025Article
- Synapse vulnerability and resilience across the clinical spectrum of dementias.Nature reviews. Neurology · 2025Review
- Synapse vulnerability and resilience underlying Alzheimer's disease.EBioMedicine · 2025Review
- Amyloid-β oligomers increase the binding and internalization of tau oligomers in human synapses.Acta neuropathologica · 2024Article
- AAGGG repeat expansions triggerScience advances · 2024Article
- Rapidly reversible persistent long-term potentiation inhibition by patient-derived brain tau and amyloid ß proteins.Philosophical transactions of the Royal Society of London. Series B, Biological sciences · 2024Article
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 2 institutions in 2 countries.
Funding
Abstract
Alzheimer's disease is the leading cause of dementia and a growing worldwide problem, with its incidence expected to increase in the coming years. Since synapse loss is a major pathology and is correlated with symptoms in Alzheimer's disease, synapse dysfunction and loss may underlie pathophysiology. In this context, this review focuses on emerging insights into synaptic changes at the ultrastructural level. The three-dimensional electron microscopy technique unequivocally detects all types of synapses, including multi-synapses, which are indicators of synaptic connectivity between neurons. In recent years it has become feasible to perform sophisticated three-dimensional electron microscopy analyses on post-mortem human Alzheimer's disease brain as tissue preservation and electron microscopy techniques have improved. This ultrastructural analysis found that synapse loss does not always precede neuronal loss, as long believed. For instance, in the transentorhinal cortex and area CA1 of the hippocampus, synapse loss does not precede neuronal loss. However, in the entorhinal cortex, synapse loss precedes neuronal loss. Moreover, the ultrastructural analysis provides details about synapse morphology. For example, changes in excitatory synapses' post-synaptic densities, with fragmented postsynaptic densities increasing at the expense of perforated synapses, are seen in Alzheimer's disease brain. Further, multi-synapses also appear to be altered in Alzheimer's disease by doubling the abundance of multi-innervated spines in the transentorhinal cortex of Alzheimer's disease brain. Collectively, these recent ultrastructural analyses highlight distinct synaptic phenotypes in different Alzheimer's disease brain regions and broaden the understanding of synapse alterations, which may unravel some new therapeutic targets.
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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.