ArticleMolecular psychiatry2025
Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer's disease.
Article in Molecular psychiatry, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 16 papers.
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Who cites it
16 citing papers in PubMed.
- Hospital-treated infection associated with Alzheimer's disease pathology: underlying mechanisms.Molecular psychiatry · 2026Review
- Integrative synaptosome multi-omics reveals disrupted synapse organization and localized cryptic transcripts in C9ORF72-frontotemporal dementia.Acta neuropathologica · 2026Article
- Early Retinal UCHL1 Dysregulation Coupled With Synaptic Loss Reflects Alzheimer's Disease Severity.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Transaldolase 1 contributes to pentose phosphate pathway disruption and synaptic dysfunction in Alzheimer's disease.Translational neurodegeneration · 2026Article
- Genetic Associations with Temporal Modeling of Alzheimer's Disease Progression Supports a Novel Paradigm for Disease Risk.medRxiv : the preprint server for health sciences · 2026Article
- ALKBH3 m1A Demethylase Deficiency Reduces Alzheimer's Amyloid-β Pathology.Advanced science (Weinheim, Baden-Wurttemberg, Germany) · 2026Article
- Progress of metabolomics-centric multi-omics research in medicine.iMetaOmics · 2026Review
- Article
- Scalable discovery of spatial multicellular patterns via neighborhood-to-sequence transformation.Communications biology · 2026Article
- A Meta-analysis to Identify Common Key Genes Across Ageing, Alzheimer's and Parkinson's Diseases.Annals of neurosciences · 2026Article
- WDR12 and HIVEP3 are contributors to cognitive preservation in Amish SuperAgers.Alzheimer's & dementia : the journal of the Alzheimer's Association · 2026Article
- Synergistic retinal UCHL1 dysregulation and synaptic vulnerability reflect Alzheimer's disease severity.bioRxiv : the preprint server for biology · 2026Article
- Network Analysis to Identify MicroRNAs Involved in Alzheimer's Disease and to Improve Drug Prioritization.Biomedicines · 2026Article
- Synthetic microbial communities: a novel emerging models for dissecting gut microbiota-host interactions in neurodegenerative diseases.Frontiers in immunology · 2026Review
- Neuroinflammatory stress preferentially impacts synaptic MAPK signaling and mitochondria in excitatory neurons.Molecular neurodegeneration advances · 2026Article
- Chemotherapy induced neurotoxicity in cancer survivors assessed through a dual database bibliometric analysis from 2005 to 2025.Discover oncology · 2025Article
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8 authors.
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Abstract
Synapse dysfunction is an early event in Alzheimer's disease (AD) caused by various factors, including amyloid beta, p-tau, inflammation, and aging. However, the precise molecular mechanism underlying synapse dysfunction in AD remains largely unknown. To understand this, we comprehensively analyzed the synaptosomes fraction in post-mortem brain samples from AD patients and cognitively normal individuals. We conducted high-throughput transcriptomic analyses to identify changes in microRNA (miRNA) and mRNA levels in synaptosomes extracted from the brains of unaffected individuals and those with AD. Additionally, we performed mass spectrometry analysis of synaptosomal proteins in the same sample group. These analyses revealed significant differences in the levels of miRNAs, mRNAs, and proteins between the two groups. To gain further insights into the pathways or molecules involved, we employed an integrated omics approach to study the molecular interactions of deregulated synapse miRNAs, mRNAs, and proteins in samples from individuals with AD and the control group, demonstrating the impact of deregulated miRNAs on their target mRNAs and proteins. Furthermore, the DIABLO analysis revealed complex relationships among mRNAs, miRNAs, and proteins that could be key in understanding the pathophysiology of AD. Our study identified novel synapse-associated candidates that could be critical in restoring synapse dysfunction in AD.
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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.