Neurodegenerative disorders [e.g. Alzheimer's disease (AD) and Parkinson's disease (PD)] are a group of devastating conditions that are caused by progressive death of neurons in different regions of the brain. On the other hand, multiple sclerosis (MS) is the most common autoimmune disease of the central nervous system, resulting in oligodendrocytes death and demyelination. Our lab primarily focuses on central nervous system (CNS) cell signaling that leads to neuronal death in Parkinson's disease (PD) and Alzheimer's disease (AD) and demyelination in multiple sclerosis (MS). All these disorders are characterized by activation of CNS glial cells (astroglia and microglia), excessive production of different proinflammatory molecules within the CNS, and death of either oligodendroglia (MS) or neurons (AD and PD). From several angles, we have been investigating mechanisms by which glial cells are activated to release different proinflammatory molecules and neurotoxins for inducing apoptosis and cell death in neurons and oligodendroglia. We are also involved in identifying signaling pathways by which glial cells may be redirected to produce neuroprotective molecules and neural stem cells could be driven towards neurons and myelin-producing cells (oligodendrocytes) within the neurodegenerative CNS. Finally, we are trying to suppress neurotoxic signaling pathways and/or boost neuroprotective signaling pathways in different animal models of neurodegenerative diseases by nontoxic drugs in order to achieve neuroprotection. Since many veterans are suffering from dementia, AD, PD, and MS, results from these studies will directly help veterans. 1
Our lab primarily focuses on central nervous system (CNS) cell signaling that leads to neuronal death in Parkinson's disease (PD) and Alzheimer's disease (AD) and demyelination in multiple sclerosis (MS). We will try to suppress neurotoxic signaling pathways and/or boost neuroprotective signaling pathways in different animal models of neurodegenerative diseases by nontoxic drugs in order to achieve neuroprotection and functional recovery. 1
