Timespan: Management of chronic cardiometabolic disease and treatment discontinuity in adult ADHD Patients.
- Subaward PI: Faraone
- TIMESPAN's main objective is to advance the management of patients with Attention Deficit Hyperactivity Disorders (ADHD) and co-occurring cardiometabolic disease by improving available treatments and risk stratification. Emerging evidence points at substantial comorbidity and shared genetics between adult ADHD and cardiometabolic diseases (i.e., Obesity, Type-2 Diabetes and cardiovascular disease).
The ADHD Evidence Project
- PI: Faraone
- The ADHD Evidence Project's goal is to disseminate curated evidence about the nature, diagnosis, and treatment of ADHD to mental health professionals, primary care professionals (PCPs), and the public.
Genetic Predictors, Transcriptomic Biomarkers, & Neurobiological Signatures of Resilience to Alzheimer's Disease.
- PIs: Faraone, Glatt
- The goal of this project is to identify genes, molecules, and brain structures that protect some people from their otherwise-elevated risk for Alzheimer’s disease. The approach we have devised for identifying resilience factors is straightforward yet, to our knowledge, unprecedented. We identify unaffected individuals at the highest levels of multivariate risk, match them to affected individuals at equivalent levels of risk, and contrast these two subgroups to find residual variation associated with the absence of disease. In this project, we will capitalize on the wealth of existing high-throughput AD risk-factor results and data, and our involvement in many of the world’s largest AD consortia, to efficiently map resilience to AD at three levels (genetics, transcriptomics, and neuroimaging), and to integrate across these levels.
SLE Treatment with N-acetylcysteine.
- PI: Perl, Faraone (Biostatistician)
- The goal of this project is to identify genes, molecules, and brain structures that protect some people from their otherwise-elevated risk for Alzheimer’s disease. Systemic lupus erythematosus (SLE) is an autoimmune disease of unknown etiology with mortality still approaching 10% in 5 years. The leading cause of death in SLE are infections due to the toxicity of immunosuppressant medications. Therefore, a significant unmet need exists for effective and non-toxic medications to treat SLE. Our central hypothesis has been formulated on the basis that effective treatment should target key checkpoints of pathogenesis, such as the depletion of reduced glutathione (GSH), which underlies the activation of the mechanistic target of rapamycin (mTOR) and inflammatory lineage specification of T cells, B-cell activation and antinuclear autoantibody production in SLE.