Nicholas William Wood

This paper introduces ASA-PD, an imaging method to detect and map α-synuclein oligomers in Parkinson's disease brain tissue, revealing a specific subpopulation of nanoscale oligomers as an early hallmark of the disease.

This paper introduces a non-invasive imaging framework combining qMRI and SRT to infer molecular features in neurodegeneration.

The paper identifies splicing dysregulation in Parkinson's disease linked to TDP-43 loss of function and shows its association with genetic mutations and cellular models.

The paper identifies microglial activation and alpha-synuclein oligomers as drivers of early neuroinflammation in Parkinson's disease using transcriptomic and aggregate profiling in early-stage brain samples.

The paper maps α-synuclein oligomers in Parkinson's disease brain tissue to identify aggregation-susceptible cells and proposes a population-level model for early pathology.

TX2P integrates transcriptomic and proteomic data to identify novel protein-coding transcripts and link RNA discoveries with protein function in epilepsy-associated genes.

This study compares molecular and cellular signatures of Parkinson's disease and Parkinson's disease with dementia using single-nuclear transcriptomics, finding distinct gene expression patterns and biological pathways.

This study uses bulk and single nuclear RNA-sequencing to analyze transcriptomic changes in repeat expansion ataxias, revealing distinct non-neuronal cell type-specific disease signatures across the human brain.

The paper shows ancestry-specific gene expression in monocytes mediates neurodegenerative disease risk through innate immune cell expression of neurodegeneration-related genes.

The paper reports genetic findings from a UK-wide study of early-onset and familial Parkinson's disease, identifying pathogenic variants in known PD genes and highlighting the need for further monogenic causes.

The paper shows that sequencing ambiguity between GBA1 and its pseudogene GBAP1 affects transcriptomic analysis, revealing non-lysosomal functions in the brain and widespread annotation inaccuracies.

The paper investigates ligand-receptor interactions (LRIs) in neurological diseases and finds that 96.8% of disease-associated LRIs are interconnected, highlighting their role in disease comorbidity and potential drug targets.

This study identifies six novel genetic loci associated with Parkinson's disease mortality and motor progression using genome-wide survival analysis.

The paper identifies novel SNCA transcripts in human dopaminergic neurons and demonstrates their impact on antisense oligonucleotide therapy for Parkinson's disease.

This study uses Mendelian randomization to investigate the causal role of lipids and statin interventions on multiple sclerosis risk and severity, finding HDL-C increases risk while RAC2 reduces it.

The paper identifies KAT8 and KANSL1 as regulators of PINK1-mitophagy linked to Parkinson's disease risk, suggesting a novel pathway for therapeutic targeting.

The paper identifies human-lineage-specific genomic elements, called CNCRs, and shows their enrichment in neurological disease genes and APOE intron-3 retention transcripts in Alzheimer's disease.

The paper identifies bi-allelic variants in TSPOAP1 as a cause of autosomal recessive dystonia, showing different clinical presentations based on variant type.

This study demonstrates that whole genome sequencing can effectively detect repeat expansions in neurological disorders with high sensitivity and specificity, enabling diagnosis in previously undiagnosed patients.

This paper identifies genetic variants associated with cognitive and motor progression in Parkinson's disease using GWAS and longitudinal cohort data.

This study uses Mendelian randomization to identify 23 potential drug targeting mechanisms for Parkinson's disease, including four drug repurposing opportunities and two drugs that may increase PD risk.

The paper examines DNM3 and VAMP4 as genetic modifiers of LRRK2 Parkinson's disease, finding no significant effect of DNM3 on age at onset but a possible interaction between LRRK2 and VAMP4.

This study identifies cell-type-specific expression of dystonia-associated genes and links them to shared genetic and biological mechanisms with psychiatric disorders.

The paper identifies disease-relevant regulatory loci in human basal ganglia using genomic and transcriptomic data from 117 brains, highlighting splicing eQTLs and ASE analyses as sources of cell-specific regulatory information.

Across 37,688 Parkinson's cases, 18,618 proxy-cases and 1.4M controls, 90 risk signals map to 78 loci (37 new); an 1805-variant polygenic score explains 26-36% of heritability.

This paper applies Mendelian randomization to identify causal factors for Parkinson's disease using 5,839 exposures and reports twelve causal associations, including adiposity.

This paper integrates eQTL and Parkinson’s disease GWAS data to identify 11 disease genes and pathways involved in PD risk through colocalisation, TWAS, and network analysis.

This study connects Parkinson’s disease heritability to cell-type-specific gene regulation, finding enrichment in lysosomal genes in astrocytic and microglial subtypes rather than specific cell types or brain regions.