Vivek Swarup

FORGE is a configurable Nextflow pipeline for snMultiome analysis that integrates snRNA-seq and snATAC-seq data through latent-variable models and enables regulatory network inference and differential testing.

The paper constructs a single-nucleus transcriptomic atlas of Alzheimer's disease and identifies cell-type-specific molecular subtypes and therapeutic targets using a new framework.

This paper shows that spinal cord oligodendrocyte metabolic changes after injury lead to β-amyloid production and chronic pain.

The paper identifies age-related dysregulation of transcription networks in oligodendrocyte differentiation using single-nucleus RNA and ATAC sequencing in mice, with parallels in MS lesions.

This study uses single-nucleus multi-omics to identify shared and distinct regulatory pathways in Pick's and Alzheimer's disease, revealing disease-specific enhancers and TF binding patterns.

The paper compares gene expression divergence between male and female germlines in Drosophila species using single-nucleus RNA-seq, finding cell-type-specific patterns and X chromosome enrichment.

This study shows that lack of m6A methylation in Schwann cells causes demyelination and regenerative failure in mice.

The paper compares proteome and transcriptome changes in DSAD brains to AD and healthy controls, finding elevated APOE in specific cell types.

The paper shows that a triple combination of HDAC inhibitor and excipients improves microglial function in a mouse model of Kabuki Syndrome by restoring chromatin marks and cognitive responses.

The paper develops a mouse model to specifically target disease-associated microglia (DAMs) using an inducible Cre system and validates its specificity through spatial transcriptomic analysis.

The paper investigates how the APOE Christchurch variant affects microglial responses to amyloid and tau pathology in mouse models, finding it enhances plaque-related responses but suppresses tau-related inflammation.

This study examines transcriptomic changes in grafted human neural progenitor cells and host retinal cells in a retinitis pigmentosa model, identifying mechanisms for vision preservation.

This study uses spatial transcriptomics and single-nucleus RNA-seq to compare genetic and sporadic Alzheimer's Disease, finding similar spatial and cell-type specific changes between sporadic AD and AD in Down Syndrome.

This study shows that myeloid-derived β-hexosaminidase supports neuronal lysosomal function and that microglial replacement can reverse Sandhoff disease symptoms.

The paper identifies the cellular origins and functional changes of astrocytes forming protective borders around CNS injuries, showing their role in neuroprotection.

The paper uses single-nucleus RNA-sequencing to compare non-enhancing and contrast-enhancing regions of high-grade gliomas, finding distinct cellular states and microenvironment features in NE regions.

This study identifies a distinct CNS regeneration program activated by integrin expression in spinal cord sensory neurons, differing from PNS regeneration and involving ubiquitination, autophagy, and signaling pathways.

This paper introduces hdWGCNA, a framework for analyzing co-expression networks in high-dimensional transcriptomics data, demonstrating its application in identifying disease-relevant modules in single-cell datasets.

This study compares HD astrocytes from human iPSCs and mouse models, identifying dysregulated synaptogenesis, actin signaling, and maturation, with unique human findings and potential therapeutic targets.

The paper identifies gene expression signatures in Alzheimer's disease neurons with tau aggregates, revealing shared and subtype-specific molecular changes related to synaptic function and metabolism.

This study uses snRNAseq to analyze HD mouse models and human brain tissue, identifying impaired oligodendrocyte maturation and a potential role for thiamine metabolism in disease pathology.

The paper identifies widespread transcriptomic dysregulation across multiple cortical regions in ASD, showing regional variation and genetic enrichment in synaptic and protein folding genes.

This study identifies conserved transcriptomic networks in Alzheimer’s disease by integrating multi-omics data across multiple cohorts and cell types.

This study uses iPSCs from autistic individuals to identify early neurodevelopmental differences during cortical and midbrain differentiation.

The paper identifies conserved proteomic changes in neurodegenerative dementias, distinguishing AD and PSP genetic risk modules and showing some variance in protein expression is post-transcriptional.

The paper identifies microglial gene networks linked to dementia risk genes that drive chronic inflammation and immune suppression in neurodegenerative diseases.

Coexpression meta-analysis of 2114 human brain RNA-seq samples across the AMP-AD consortium identifies five consensus Alzheimer's disease transcriptional clusters, including two sex-heterogeneous clusters and a previously unreported proteostasis cluster.

This study develops an inducible mouse model of Friedreich’s Ataxia to investigate reversible phenotypes by modulating frataxin levels and observing functional recovery.