According to the United Nations, the majority of the world’s population is growing older, in 2000, 10% of the total population of the world was over 60 years old and is projected to increase to 21% by 2050. The single most important societal threat to the ageing population is the cognitive decline resulting in loss of dignity, independence, and enormous pressure for resources. 

The Jadavji Laboratory investigates neurological diseases of aging, such as stroke and dementia. We use an interdisciplinary approach to tackle these complicated human diseases. Using both in vitro and in vivo tools, the Jadavji laboratory will work towards understanding the development and mechanisms associated with diseases of aging. We also investigate comorbidities, interactions with other diseases, and therapeutic options for diseases of aging. 

Models of Disease 

Our contributions to nutritional neuroscience aging research include providing an understanding on how increased levels of B-vitamins and choline can promote recovery after stroke. Furthermore, after ischemic stroke we have discovered that dietary deficiencies in vitamin B12 increase apoptosis in brain tissue and change mitochondria metabolism, specifically the TCA cycle in brain tissue. Our work has also focused on changes in the gut after ischemic stroke, we have shown that a dietary vitamin B12 deficiency prior to stroke impacts dysfunction in B12 transport.  

We have also demonstrated that a maternal diet deficient in either choline or folic acid negatively impacts ischemic stroke outcome in male and female offspring. We have also described changes in the gut of the offspring, using untargeted metabolism. Our work has demonstrated that female offspring were impacted more with specific changes in the cholesterol metabolism and neuroprotection.  This work has focused on behavioral outcomes, brain tissue analysis, metabolism, and flow within the brain and body. 

In normal brain tissue we have demonstrated that when there is a genetic deficiency in one carbon metabolism or dietary folic acid intake, choline is used to compensate. Furthermore, we have also shown that one-carbon metabolism plays an important role in the hippocampal function and morphology. 

Using the Drosophila melanogaster model we have demonstrated that increased dietary intake can have a negative impact of health outcomes post hypoxia. These health outcomes include mortality and climbing behaviors. 

Our research has been funded by the USDA National Institute of Food and Agriculture, American Heart Association, Arizona Department of Health Sciences, Arizona Alzheimer’s Consortium, and the Burroughs Wellcome Fund.