CTF Consortium Member

Amantha has served as the Assistant Professor of Neurobiology at the University of Pittsburgh School of Medicine since 2016. She has been the recipient of the Cornelli Young Investigator Award for research in Alzheimer’s Disease and the Memory Loss in Alzheimer’s Disease (MEMOSAD) Award.

Amantha has produced many publications and is passionate about finding a cure for dementia such as Alzheimer’s disease, with her work focused on the Role of GPCRs in the AD brain.

Alzheimer's disease is the most common type of dementia in people aged 65 or older and is one of the biggest medical and social challenges of our generation. Of the top ten leading causes of death worldwide, Alzheimer's disease is the only one that we cannot prevent, cure, or slow down.

In the United States alone, 5.3 million people have Alzheimer's disease, and ~480,000 new cases are diagnosed each year. Several approved drugs ameliorate some of the symptoms of Alzheimer's disease. Unfortunately, no current intervention strategy can modify the underlying disease mechanisms. Therefore, a major challenge for the future is to gain a clearer understanding of disease mechanisms in order to develop effective therapeutic strategies.

Alzheimer’s disease is clinically characterized by progressive brain cell loss and inflammation, memory impairment, cognitive deficits, and behavioral changes. Postmortem studies of the brains from patients reveal two pathological hallmarks of the disease: (1) amyloid plaques, composed of aggregates of the amyloid-beta protein, and (2) neurofibrillary tangles, composed of aggregates of the tau protein.

An imbalance between the production and clearance of amyloid-beta initiates a cascade of events, progressively leading to tau pathology, inflammation, brain cell loss, and, consequently, memory loss. A major challenge for the future is to gain a clearer understanding of disease mechanisms in order to develop effective therapeutic strategies.

In collaboration with Clear Thoughts Foundation, we propose to determine GPCR profile in control and AD patient brain samples to establish the repertoire of aberrantly regulated GPCRs in AD. We will then investigate the functional relevance of changes in GPCR expression on amyloid pathology in in vitro and in vivo Alzheimer’s disease models. We anticipate that these studies will lead to novel insights into the role of GPCR in Alzheimer’s disease and identify putative novel therapeutic targets for Alzheimer’s disease.

For a more in-depth overview of Thathiah's previously funded research (2017 and 2018) and to explore the basis of which her CTF Consortium research stems, view her

Research Page.

Further discoveries through this research will work toward developing therapeutic intervention strategies to treat Alzheimer’s disease and other related dementias.