Peter St George‐Hyslop

This paper identifies APOE-ϵ4-induced fibronectin accumulation at the blood-brain barrier as a key mediator of astrocyte-endothelial dysfunction in Alzheimer's disease, highlighting it as a potential therapeutic target.

This study shows how non-coding variants in CD33 affect Alzheimer's risk by altering CD33M dimerization and interactions with clusterin and Aβ, impacting microglial function.

This study identifies CD45 as a sialic acid-dependent binding partner of CD33, showing that their interaction contributes to Alzheimer's disease susceptibility through impaired microglial function.

This study investigates how DNA partitioning affects the phase behavior and dynamics of FUS condensates, revealing its role in modulating liquid-to-solid transitions and microstructure over time.

This study investigates how the fusion of biomolecular condensates, influenced by ageing and mixing rates, leads to the formation of multiphase structures with distinct material properties.

The paper investigates how mutations in the FUS protein affect axonal cytoskeletal organisation in ALS/FTD models, finding reduced actin density and axonal branch complexity.

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.

The paper develops a multiplex reverse genetics platform to identify genetic modifiers of protein misfolding in neurodegenerative diseases and identifies DNAJB6 as a modifier of toxicity and solubility of ALS/FTD-linked RNA-binding proteins.

The paper identifies three SNVs associated with delayed age at onset of cognitive impairment in Amish populations, with one replicated in an independent dataset and linked to the SHISA6 gene.

This study shows that TYROBP-APOE signaling in microglia can occur without TREM2 and influences AD pathology in mouse models.

This paper identifies five new genetic risk loci for Lewy body dementia through whole-genome sequencing and shows shared risk profiles with Alzheimer’s and Parkinson’s disease.

This study shows TET2 regulates microglial inflammatory responses through NF-κB-dependent pathways and metabolic changes, suggesting it as a target for neurodegenerative diseases.

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.

Genetic correlations across 25 brain disorders (215,683 cases) reveal broad psychiatric common-variant sharing, largely distinct neurological disorders, and migraine as the only significant cross-category link.

The paper identifies a genetic variant near CXCR4 associated with increased risk for PSP and PD, showing dysregulation of CXCR4 and microglia-related genes in neurodegenerative diseases.