Role of classical complement pathway underling glial phenotypes and multiple pathologies in Alzheimer’s disease and cerebrovascular disease
Aim 1 Determine how transcriptional risk profiles of inflammatory genes and their interaction with APOE genotype contribute to synaptic loss, neuroinflammation, cerebrovascular disease, and tau pathology in AD.
Aim 2 Determine glial and neuroinflammatory phenotypes associated with AD and cerebrovascular disease and validate the findings from Aim 1 using the newly defined phenotypes together with traditional pathological measures
Aim 3 Validate clinical implications of the findings from Aims 1 and 2 with longitudinal trajectory of biomarkers and neuropsychological cognitive functions in the larger FHS cohort.