Paramita Chakrabarty, Ph.D.

Dr. ChakrabartyAssistant Professor

Department of Neuroscience
Center for Translational Research in Neurodegenerative Disease (CTRND)
1275 Center Drive
PO Box 100159
Gainesville, FL  32610-0159
Office: 352-273-7271
Lab: 352-294-8764




2003 Ph.D.
(Biochemistry & Molecular Biology)
Jawaharlal Nehru University
New Delhi, India
2003-2005 Postdoctoral Fellowship
University of Washington
Seattle, WA
2005-2009 Postdoctoral Fellowship
Mayo Clinic
Jacksonville, FL
2009-2011 Postdoctoral Fellowship
University of Florida
Gainesville, FL

Key Words: Neuroinflammation, Alzheimer’s disease, Parkinson’s disease, Amyloid β, APP, Tau, Synuclein, Cytokine, Selective Neurodegeneration, Innate Immune Response, Microglia, Transgenic Mice

Research Summary:

My research focuses on understanding the role of immune activation in dementias of the elderly, such as Alzheimer’s disease, Parkinson’s disease and tauopathies. During the course of my studies, I (along with my collaborators) coined the term immunoproteostasis. This refers to the constantly evolving and complex inter-relationship between innate immunity and proteostasis in the brains of mouse models of neurodegenerative diseases. For example, through a systematic evaluation of inflammatory and anti-inflammatory regimens, I have shown that contrary to a persistent dogma, innate immune activation is not amyloidogenic in an Alzheimer mouse model. On the other hand, inflammatory activation can reduce amyloid burden in mouse models of Alzheimer’s disease, whereas anti-inflammatory signaling increases amyloid burden through a multitude of mechanisms. One of these pathways involves upregulation of Apolipoprotein E protein, which is the one of the most significant genetic determinants of sporadic Alzheimer’s disease. Other areas of research in my laboratory include applying the concept of immunoproteostasis in mouse models of tauopathy and synucleinopathy to understand the pathogenesis of these diseases. Much of my work focuses on using recombinant adeno-associated viruses as a means of generating somatic brain transgenesis models that serve as phenotypic screens for evaluating potential immune targets in the brain as well as to understand the mechanism of immune function in altering proteostasis.

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