Obesity is a major public health problem that affects approximately 30% of US adults. There is a growing body of evidence supporting the idea that obesity-induced metabolic stress is associated with significant neural and cognitive deficits in addition to its negative impacts on the rest of body, and that these cognitive deficits often increase with age.

We previously demonstrated that metabolic stressors induced by obesity lead to similar biochemical, morphological, electrophysiological and behavioral phenotypes as those seen in animal models of dementia or Alzheimer’s disease (AD).

Moreover, we have shown that these phenotypic changes are associated with the loss of inositol polyphosphate multikinase (IPMK) in the cortex and hippocampus, suggesting that the loss of this nutrient sensing protein contributes to these phenotypes.

One of the long-term objectives of this laboratory is to determine the cellular underpinnings of metabolic stress-induced cognitive dysfunction, with the ultimate goal of developing novel interventions.

Other relevant projects include:

1. The role of the inositol pathway in energy metabolism.
2. The effects of metabolic imbalance on neuronal function and various neuropsychiatric conditions
3. The role of CNS (central nerve system) metabolic genes on affective disorders.
4. The effects of atypical antipsychotic drugs on metabolic imbalance
5. The role of lipid pathways on oligodendrocyte differentiation