Decoding early synaptic failure through multiomics

Synapse dysfunction is one of the earliest and most critical events in Alzheimer’s disease and emerges well before widespread neurodegeneration or clinical symptoms. While amyloid β, tau pathology, inflammation, and aging are well-recognized contributors, how these factors converge across multiple molecular layers to disrupt synaptic regulation remains an open question.

In this webinar, we showcase a comprehensive, integrated multiomic reanalysis of a synaptosome dataset from Kumar et al.1 using Illumina Connected Multiomics software. You will learn how joint analysis of mRNA and miRNA data within a single multiomic framework reveals regulatory signals that would be difficult, or impossible, to detect using single omic approaches.

We reproduce and extend the original study through a multiomic lens by:

• Profiling expression patterns of canonical synaptic and cell-type marker genes across omic layers
• Performing differential expression analyses across disease conditions using integrated datasets
• Linking miRNA and mRNA correlations to regulatory mechanisms driving synaptic dysfunction
• Placing multiomic results in biological context through pathway and disease-gene enrichment, including integration with Illumina Correlation Engine

Throughout the session, we focus on practical, reproducible multiomic workflows and demonstrate how Connected Multiomics enables coordinated analysis across data types to uncover cell-type–specific stress responses, regulatory programs, and disease-relevant pathways in Alzheimer’s disease research.

^[1] Kumar, Subodh, et al. "Integrated multi-omics analyses of synaptosomes revealed synapse-associated novel targets in Alzheimer’s disease." Molecular Psychiatry (2025): 1-16.

For Research Use Only.  Not for use in diagnostic procedures.

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