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Alzheimer’s disease (AD) is the most common form of dementia in the elderly population. The main pathological features of AD are progressive loss of nerve cells and deposition of abnormal protein aggregates called senile plaques (SP) and neurofibrillary tangles (NFTs). Studies in animal and cell models have shown that both plaques and tangles cause nerve damage leading to loss of cognitive functions. The main focus of Professor Paudel’s laboratory is to elucidate the molecular mechanisms by which SPs and NFTs are formed and how these two protein aggregates cause neurodegeneration leading to cognitive loss. There is no effective treatment for AD. Our long-term goal is to identify therapeutic molecular targets for treatment of AD.
Hemant K. Paudel’s research focuses on the following:
The specific research areas in the laboratory include:
Duan, J. Marcellus, K. A., Qin, X. Wang, Y and Paudel, H. K. (2018) Mol and Cell. Neurosci 89, 1-8.
Qin, X. Wang, Y. and Paudel, H.K. (2016) J. Biol. Chem. 291, 22276-22287.
Ryen MacDonald, Sebastien Barbat-Artigas, Chulmin Cho, Huashan Peng, Jijun Shang, Ayman Moustaine, Salvatore Carbonetto, Richard Robitaille, Lorraine E. Chalifour and Hemant Paudel (2017). Frontier in Aging Neurosci 9. 258.
(2017) Y. Wang et al. Neurobiology of Disease 103 (2017) 78–88.
Yunling Wang, Xike Qin and Hemant K. Paudel (2017). Oncotarget 8, 48533-48533.
Heather Pekeles, Hamid Y. Qureshi, Hemant K. Paudel, Hyman M. Schipper, Mervyn Gornistky, Howard Chertkow (2019). Alzheimer’s & Dementia: Diagnosis, Assessment & Disease Monitoring 11 (2019) 53-60.
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