- Alzheimer's disease research and treatments
- Neuroinflammation and Neurodegeneration Mechanisms
- Epigenetics and DNA Methylation
- Adolescent and Pediatric Healthcare
- Bipolar Disorder and Treatment
- Tryptophan and brain disorders
- 14-3-3 protein interactions
- Protein Kinase Regulation and GTPase Signaling
- Ubiquitin and proteasome pathways
Northwestern University
2024-2025
University of Iowa
2022-2024
Alzheimer's disease (AD) therapies utilizing amyloid-β (Aβ) immunization have shown potential in clinical trials. Yet, the mechanisms driving Aβ clearance immunized AD brain remain unclear. Here, we use spatial transcriptomics to explore effects of both active and passive brain. We compare actively patients with nonimmunized neurologically healthy controls, identifying distinct microglial states associated clearance. Using high-resolution alongside single-cell RNA sequencing, delve deeper...
Abstract Protein kinase A (PKA) neuronal function is controlled by the interaction of a regulatory (R) subunit dimer with two catalytic subunits. Recently, L50R variant in gene encoding RIβ was identified individuals novel neurodegenerative disease. However, mechanisms driving disease phenotype remained unknown. In this study, we generated mouse model carrying RIβ-L50R mutation to replicate human and study its progression age. We examined post-mortem brains affected as well live cell...
Abstract Background Recent advances in Alzheimer’s disease (AD) therapeutics involve immunization against amyloid‐β (Aβ). Post‐mortem brain analysis from the first active Aβ immunotherapy trial indicated clearance of some AD patients. Yet, mechanisms regulating following remain unknown. Method Here, we utilized a novel spatial proteogenomics approach to study tissues 13 patients immunized with Aβ. We compared these actively patient brains non‐immunized and non‐neurologic controls....
Abstract Bipolar disorder (BD) has been previously associated with premature mortality and aging, including acceleration of epigenetic aging. Suicide attempts (SA) are greatly elevated in BD decreased lifespan, biological poorer clinical outcomes. We investigated the relationship between GrimAge, an clock trained on time-to-death SA two independent cohorts individuals (discovery cohort - controls (n=50), (n=77, BD/SA) without (n=67, BD/non-SA) lifetime history SA; replication BD/SA (n=48)...