Paramita Chakrabarty, Ph.D.

Assistant Professor

Department of Neuroscience
Center for Translational Research in Neurodegenerative Disease (CTRND)

Department of Neuroscience
Center for Translational Research in Neurodegenerative Disease (CTRND)
1275 Center Drive
PO Box 100159
Gainesville, FL  32610-0159

Email:  pchakrabarty@ufl.edu
Office Phone:  (352) 273-9691
Website:  Chakrabarty Research

Education: 

2003 Ph.D.
(Biochemistry & Molecular Biology)
Jawaharlal Nehru University
New Deli, India
2003-2005 Postdoctoral Fellowship
(Pathology)
University of Washington
Seattle, WA
2005-2010 Postdoctoral Fellowship
(Neuroscience)
Mayo Clinic
Jacksonville, FL
2010-2011 Postdoctoral Fellowship
(Neuroscience)
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:
Different groups of neurons are affected in different neurodegenerative diseases such as Alzheimer’s disease, Parkinson’s disease and Amyotrophic lateral sclerosis. The reason why one population of neurons die and others are spared in these diseases remains poorly understood. Previous studies suggest that components of the innate immune system, cytokines and chemokines, may differentially affect specific group of neurons in these different diseases, ultimately leading to neuronal demise. My research focus is to investigate how innate immune signaling affects the pathology of different disease associated proteins, such as amyloid β, Tau and synuclein, leading to selective neuronal death and impaired cognition. These data will inform neuroprotective strategies against these diseases and help us guide future studies as to what determines differential vulnerability of brain regions to a wider spectrum of inflammatory stimuli.

Research Focus & Aims:
My research is focused on understanding the role of neuro-inflammation in dementias of the elderly, such as Alzheimer’s disease, Parkinson’s disease and ALS. Using this knowledge, my research team and I intend to design and develop immunobiotherapies against these inexorable diseases. Overall, data from my past research has refuted the long-held dogma that a strong pro-inflammatory stimulus creates a self-reinforcing neurotoxic feedback loop that promotes Alzheimer’s disease type neurodegeneration. Indeed, this has opened up future avenues of research in my laboratory where the current focus is to generate engineered immunobiotherapies by harnessing innate immune system components. This line of research is highly translational as this can be tailored to pharmacologic manipulations using biologics based on my research.

 

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