Yoav Ben‐Shlomo

This study investigates whether blood pressure interacts with genetic risk of dementia to influence dementia diagnosis, finding that higher systolic blood pressure increases dementia risk regardless of genetic predisposition.

This study identifies causes and consequences of vascular dementia using polygenic risk scores, phenome-wide association, and Mendelian randomization analyses from UK Biobank data, highlighting cardiometabolic and educational factors as key modifiable risks.

This paper uses Mendelian randomization to assess if existing drugs targeting lipid-lowering, anti-hypertensive, or anti-inflammatory pathways affect vascular dementia risk, finding potential benefits for beta-1 adrenergic receptor antagonists and risks for ACE inhibitors.

This study uses whole genome sequencing to identify 18 novel genetic loci associated with plasma fibrinogen levels, including variants more common in African populations and linked to liver-related traits and disease.

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

The paper applies a multivariate two-sample Mendelian Randomisation approach to estimate causal effects on disease progression intercept and slope using Parkinson's cohorts.

This paper identifies three novel genetic variants associated with levodopa-induced dyskinesia in Parkinson's disease and confirms associations with ANKK1 and BDNF, while also finding gender, age at onset, and anxiety as risk factors.

This study identifies genetic variants associated with motor progression in Parkinson's disease using GWAS and functional analysis.

This study identifies APOE-ε4 and LRP1B as genetic risk factors for Parkinson's disease dementia using genome-wide survival analysis in 3,964 PD cases.

This study uses Mendelian randomization to identify causal risk factors for Alzheimer's disease, finding that education, fluid intelligence, and physical activity are likely causal, while most associations are consequences of early disease.

This study uses Mendelian randomization to investigate causal relationships between cytokine concentrations and Alzheimer's disease risk, finding weak evidence of a causal effect for some cytokines.

This study examines how genetic risk for Alzheimer's disease affects plasma metabolites across different ages, finding strong associations with lipid traits, particularly influenced by the APOE4 isoform.

This study uses Mendelian randomization to examine bidirectional causal effects between brain morphology and Alzheimer's disease risk across different life stages.

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

This study identifies 5,552 blood-cell trait-variant associations across 746,667 individuals from 5 global populations, including 71 novel loci and ancestry-specific variants not found in European ancestry populations.

This study identifies 5,106 new genetic variants associated with blood cell traits using large-scale GWAS, highlighting the polygenic and monogenic basis of hematopoiesis.

The DPUK Data Portal provides secure access to cohort data for dementia research, supporting multi-modal analyses and collaborations across multiple institutions.

This study uses Mendelian randomization to show education and intelligence both causally lower Alzheimer's disease risk, with intelligence having an independent effect.

The paper analyzes genetic variants at the PCSK9 locus to assess their phenotypic effects on lipid levels and disease outcomes, finding concordance with PCSK9 inhibitor trials for myocardial infarction but discordance for type 2 diabetes.