Tissue Engineering and Regenerative Medicine

Arnav Gupta is passionate about exploring causal relationships of drugs commonly used to treat neurodegenerative disorder. Arnav is interested in pursuing a career in neuroscience. His passion in studying the brain and memory has inspired him to do research about Alzheimer’s disease. This common disorder presents so many unanswered questions, and Arnav is motivated to do further research in the future to answer some of these questions.\r\n\r\nResearch Interests: Neuroscience, Alzheimer disease, Stem Cells, neurodegenerative disorder\r\n

Alzheimer’s disease is a very common type of dementia that destroys memory and other important mental functions. It is a neurodegenerative disorder which affects over 5 million people in the United States alone. In fact, it is the 6th leading cause of death in the United States, and on average, an American is diagnosed with Alzheimer’s disease every 66 seconds. This can be a familial or sporadic disease which is primarily caused by the destruction of neurons which starts from the hippocampus and spreads throughout the brain (cerebellum is spared). The apoptosis of the countless neurons seems to be caused by a multitude of factors including amyloid-beta plaques, Tau tangles, and neuronal loss. For the sake of this investigation, there will be a primary focus on the amyloid-beta plaques because the accumulation or buildup of neurotoxic plaques on the neurons seems to be a key factor in Alzheimer’s disease. Enzymes called γ-secretase and β-secretase cleave a protein called an amyloid precursor protein (APP) to form these amyloid-beta peptides which can accumulate and form neurotoxic plaques. Previous studies have found that DAPT, a dipeptide analogue, is effective in inhibiting γ secretase thus decreasing amyloid-beta concentration in the brain. This study confirms the efficacy of DAPT in inhibiting γ-secretase, but also investigates the alternative inhibitory effects of other drugs like Activase® rt-PA (alteplase), a tissue plasminogen activator typically used for treatment of stroke, and clonazepam (E64), a pill used to treat panic disorder and anxiety. Although the goal was to see the effects on Aβ40 (40 amino acid amyloid-beta chain) and Aβ42 (42 amino acid amyloid-beta chain) production, only the effects of Aβ40 production were examined due to possible contamination in the Aβ42 tests.

Aditi Singh has over seventeen years of experience in research and academics. After completing her Doctorate in the year 2000 from King Georges’ Medical College, she started teaching at undergraduate and post graduate level. During PhD thesis, she tried to understand the pathogenesis of Japanese encephalitis virus in disease confirmed patients; where in pro inflammatory cytokines were studied and evaluated. Her area of research interest is Microbiology, Immunology and Enzymology. Till now, she has authored more than thirty research papers in national and international journals and two book chapters. She has presented more than twenty papers in national and international conferences. Currently, she is working as Associate Professor in Amity University, a leading private University of India.

Japanese encephalitis (JE) is one of the chief causes of acute encephalitis syndrome (AES) in North India with more than 15% confirmed cases. The disease is caused by Japanese encephalitis virus (JEV), a neurovirulent RNA flavivirus transmitted by Culex mosquitoes. The virus in natural cycle circulates between pig and mosquitoes or bird and mosquitoes, with pigs being the most important biological amplifiers. Though humans are accidental dead end hosts, JE has generated considerable public anxiety because it mainly remains a disease of children. The disease ranges from non-specific febrile illness to a severe meningoencephalomyelitis illness. The transmission of disease can occur throughout the year in endemic zone, with disease at a peak during monsoon season. Since there is no specific treatment available and vaccination is the best measure to get protection from the disease; it is important to understand the molecular mechanisms in host. The virus has been shown to induce neutrophil infiltration in neural and extra neural tissues. A neutrophil chemotactic protein derived from macrophages had been isolated from JEV induced animal models. It had variety of pathologic effects on host, including vascular permeability and breach in blood brain barrier. The presence of inflammatory chemokine IL-8 was also significantly detected in JE confirmed patients during acute phase of illness. The study had revealed \r\na correlation between IL-8 levels and severity of illness as all severely ill and fatal cases showed higher levels of IL-8 in acute cerebrospinal fluid (CSF) and serum. In cases who recovered completely, the level of IL-8 declined markedly by convalescent phase. The study indicates important interaction between pro inflammatory cytokine, macrophages and neutrophils during JE infection.