Simon Lovestone

The paper develops a multivariate methylation risk score using blood DNA methylation data to predict dementia risk and cognitive impairment in Alzheimer's and Parkinson's disease cohorts.

This study shows iPSC-derived astrocytes from AD patients reflect key pathophysiological features, offering a new model for AD research and therapeutic screening.

This study examines APOE Christchurch carriers in UK Biobank to assess their risk of Alzheimer's disease, cardiovascular disease, and dyslipidemia, finding lower apoB levels and reduced AD risk.

The paper uses induced pluripotent stem cell-derived cortical neurons from early Alzheimer's patients to show that cellular vulnerability to amyloid-beta correlates with clinical vulnerability.

This study performs GWAS on quantitative AD biomarkers and cognitive traits, identifying new loci associated with memory performance and cognitive decline.

The paper identifies genetic and epigenetic factors influencing plasma protein levels linked to Alzheimer's disease, finding novel associations with TREM2 and TBCA.

The paper conducts GWAS on CSF Alzheimer's disease biomarkers, identifying genetic associations with NF-L, YKL-40, and Ng levels.

This study identifies shared transcriptomic changes between Alzheimer's disease and Major Depression in mice, suggesting Major Depression may be an early manifestation of Alzheimer's.

The paper conducts a genome-wide association study (GWAS) on Alzheimer’s disease CSF biomarkers in the EMIF-AD dataset, identifying novel genetic signals and confirming existing associations.

This study investigates how Tau pathology in early Alzheimer's disease affects neurophysiological network dynamics using MEG and PET scans, finding frequency-specific correlations between Tau levels and network efficiency and segregation.

The paper estimates brain age gaps using MRI and machine learning in individuals with and without brain disorders, finding heritability and genetic overlap with common disorders.

This study performs a large GWAS of Alzheimer's disease, identifies four new risk loci, and highlights pathways involving immunity, lipid metabolism, and APP/Aβ processing.

The paper identifies 25 genetic loci associated with subcortical brain structure volumes in over 40,000 individuals, revealing novel biology and potential drug targets.

The paper combines GWAS, clinical data, and experimental models to identify JAK-STAT pathway dysregulation as a potential therapeutic target for Alzheimer’s disease.

This study shows that serum from MCI patients predicts AD conversion up to 3.5 years before diagnosis by altering hippocampal progenitor cell behavior.