Owen A. Ross

This study shows that PINK1 loss in astrocytes causes inflammation and neuronal death through non-cell-autonomous mechanisms, and that autophagy enhancement can reverse these effects.

This study identifies miRNA biomarkers in brain-derived extracellular vesicles from plasma to distinguish Lewy body disease from Alzheimer's disease with high accuracy.

This study conducts a GWAS on Pick's disease and identifies two SNPs associated with risk, though not at genome-wide significance, suggesting potential genetic factors beyond MAPT mutations.

The paper investigates genetic and causal links between post-traumatic stress disorder and rapid-eye-movement sleep behavior disorder using polygenic risk scores, genetic correlation, and Mendelian randomization analyses.

The paper identifies PPM1M as a phosphatase that reverses LRRK2-mediated Rab phosphorylation and links a rare mutation to Parkinson's disease.

This study examines the distribution of α-synuclein oligomers in LRRK2-related Parkinson's disease, finding a negative correlation between oligomers and Lewy-related pathology.

This study identifies genetic risk factors for FTLD-TDP subtypes using whole-genome sequencing and meta-analysis across multiple cohorts.

This study identifies six genetic loci associated with progressive supranuclear palsy, including a novel locus, and links them to oligodendrocytic dysfunction and C4A expression.

This study uses whole-genome sequencing to identify new genetic loci and structural variants associated with progressive supranuclear palsy, including novel signals in APOE and H1/H2 haplotype region variants.

The paper identifies miR-29 and ATG9A as regulators of mitophagy and discovers EOPD-linked variants in ATG9A.

This paper performs a large meta-analysis of GWAS in dementia with Lewy bodies, identifying sex-specific genetic risk signals and highlighting the need for larger cohorts.

This study identifies genetic modifiers of LRRK2 mutations in Parkinson's disease, finding a significant variant in CORO1C and a polygenic risk score effect on penetrance.

The paper identifies SERPINA5 as a novel tau binding partner in Alzheimer's disease by analyzing hippocampal gene expression and neurofibrillary tangles.

The paper identifies four genes, including two novel ones, co-expressed with TREM2 in Alzheimer's disease using whole-exome data from ADSP.

This study investigates associations between mitochondrial genomic variation and risk of Corticobasal Degeneration (CBD) and Progressive Supranuclear Palsy (PSP), as well as tau pathology measures in PSP.

The paper investigates RNF213 variation's role in neurovascular diseases across Caucasian and Japanese populations, finding linkage disequilibrium between SLC26A11 and RNF213 variants associated with ischemic stroke and aneurysms.

The paper identifies common LRRK2 locus variation associated with survival in progressive supranuclear palsy, linking it to gene expression regulation and suggesting therapeutic implications for tauopathies.

This study identifies SNCA risk variants specific to RBD and overt synucleinopathies, finding distinct associations and opposite effects at the 3' end of SNCA.

The paper combines exome sequencing and array-based comparative genomic hybridization to identify genetic risk factors in familial Parkinson’s disease, finding novel SNVs and CNVs.

The paper identifies dark and camouflaged gene regions in the human genome, shows how long-read sequencing reduces their prevalence, and applies an algorithm to uncover disease-relevant variants in Alzheimer's Disease Sequencing Project data.

This study estimates the heritability of dementia with Lewy bodies (DLB) and finds it to be higher than previous estimates, with low variance explained by polygenic risk scores from Parkinson's or Alzheimer's disease.

The paper identifies Parkinson's risk variants in a SNCA enhancer by analyzing open chromatin in mouse dopamine neurons and validates their function in zebrafish and mice.

This study identifies genetic overlaps between frontotemporal dementia and immune-mediated diseases, finding strong enrichment with rheumatoid arthritis and moderate enrichment with other immune conditions.