Neurologic Diseases

Center researchers will elucidate mechanisms underlying multiple neurologic diseases: Multiple Sclerosis; Alzheimer’s disease; ALS; and chronic inflammatory pain. Multiple Sclerosis is a debilitating inflammatory disease of the central nervous system (CNS) that has genetic, infectious, and environmental triggers. Neurodegenerative diseases including Alzheimer’s disease and ALS are becoming an increasing burden to society and the health-care system. Chronic pain is a major problem to health-care providers today, with few existing treatments. In all these diseases, inflammation may cause induction and expression of the disease. We will investigate how interactions between the immune system and the nervous system can drive changes in neuronal activity, survival, and central nervous system health.  

The Weiner Lab is examining the role of nervous system immune cells, known as microglia, in inflammation related to Alzheimer’s disease (AD), multiple sclerosis (MS) and ALS. Microglia normally regulate inflammation in nerve cells by increasing inflammation in response to infection, but then eliminating it when the immune response is no longer needed. However, AD is associated with persistent inflammation and Dr. Weiner will examine how microglial cells mediate immune responses from a number of genetic perspectives. In MS and ALS microglia lose their protective role and may also become toxic.

Having identified a unique genetic signature for microglia, the Weiner Lab uses this signature to study the role of microglia in MS, ALS and AD mouse models and in humans in their research at the Evergrande Center. Using a technique that reverses the expression of pro-inflammatory microglial genes, the Weiner Lab will examine how the expression of those genes affects microglial cell uptake of Abeta, a molecule found in the brains of AD patients. Continuing their current research on how Abeta dramatically affects inflammatory gene expression, they will identify factors that regulate gene expression, establishing a basis for therapeutic treatments that modulate the relationship between Abeta and microglia. These findings will also be applied to progressive forms of multiple sclerosis and to ALS.