Preclinical Alzheimer’s disease
Focus on cognitively unimpaired individuals at elevated risk, with longitudinal follow-up of cognition, biomarkers, imaging, and genetic risk factors.
Research program
Alzheimer’s disease mechanisms before symptoms begin.
ADGEN investigates how inflammation, tau biology, synaptic vulnerability, genetics, imaging, and cognition converge during the presymptomatic phase of Alzheimer’s disease.
Research pillars
A multi-scale translational program
Neuroinflammation and innate immunity
Study inflammatory regulators and immune pathways that may act upstream of tau pathology, synaptic dysfunction, and cognitive decline.
Tau pathology and synaptic integrity
Investigate how phosphorylated tau species, synaptic proteins, and imaging markers converge to predict early vulnerability.
Biomarker discovery
Integrate CSF, plasma, proteomic, and imaging biomarkers to identify disease trajectories and biologically meaningful risk profiles.
Genetics, ApoE biology, and pharmacogenomics
Preserve the historical strength of ADGEN in ApoE biology, lipid metabolism, pharmacogenomics, and genetic susceptibility.
Multiomics and systems neurobiology
Use proteomics, genomics, transcriptomics, and gene expression datasets across PREVENT-AD, ADNI, ROSMAP, and related cohorts.
Mechanistic focus
Inflammation → tau → synaptic dysfunction → cognition
A central ADGEN hypothesis is that specific inflammatory regulators contribute to early tau-related biology and synaptic vulnerability during the silent phase of Alzheimer’s disease. The program tests this model across CSF and plasma biomarkers, PET/MRI imaging, cognition, gene expression, and replication cohorts.
InflammationTau biologySynaptic dysfunctionCognition