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Avik Roy
Graduate Student
1735 W Harrison Street
Cohn Research Building # 336
Rush University Medical Center
Ph: (312)9423167
Email: avik _roy@rush.edu
Received M.S. from the University of Calcutta in biochemistry (1999-2001) and
currently pursuing Ph.D in Pahan lab.
Research interest
My area of research highlights microglial activation in different
neuroinflammatory diseases and a possible therapeutic approaches to modify
activated microglia towards its neuroprotective function. In neurodegenerative
condition, microglia produce different proinflammatory cytokines and reactive
oxygen species which cause demyeliantion and finally,neuronal loss. On the
other hand, microglia can also produce a large amount of neurotrophic factors
such as BDNF, NT-3 etc. We have found that nitric oxide as one of the key
component which regulates microglia mediated neuroinflammation in brain.
Different proinflammatory molecules such as IFN-γ, TNF-α, IL-1β, HIV coat
protein gp120 etc and autoimmune T cells induce microglial activation via nitric
oxide. However, in our recent studies we showed that activated microglia could
be switched to produce different neuroprotective factors in the presence of drug-
modified autoimmune T cells.
Publications
pubmed
Graduate Student
1735 W Harrison Street
Cohn Research Building # 336
Rush University Medical Center
Ph: (312)9423167
Email: avik _roy@rush.edu
Received M.S. from the University of Calcutta in biochemistry (1999-2001) and
currently pursuing Ph.D in Pahan lab.
Research interest
My area of research highlights microglial activation in different
neuroinflammatory diseases and a possible therapeutic approaches to modify
activated microglia towards its neuroprotective function. In neurodegenerative
condition, microglia produce different proinflammatory cytokines and reactive
oxygen species which cause demyeliantion and finally,neuronal loss. On the
other hand, microglia can also produce a large amount of neurotrophic factors
such as BDNF, NT-3 etc. We have found that nitric oxide as one of the key
component which regulates microglia mediated neuroinflammation in brain.
Different proinflammatory molecules such as IFN-γ, TNF-α, IL-1β, HIV coat
protein gp120 etc and autoimmune T cells induce microglial activation via nitric
oxide. However, in our recent studies we showed that activated microglia could
be switched to produce different neuroprotective factors in the presence of drug-
modified autoimmune T cells.
Publications
pubmed
