Browsing by Author "Maitrayee Sinha"

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Ceramide and sphingosine-1-phosphate in cell death pathways: Relevance to the pathogenesis of Alzheimer’s disease
(Bentham Science Publishers B.V., 2016) Sankha Shubhra Chakrabarti; Aritri Bir; Jit Poddar; Maitrayee Sinha; Anirban Ganguly; Sasanka Chakrabarti
The metabolic turnover of sphingolipids produces several signaling molecules that profoundly affect the proliferation, differentiation and death of cells. In particular, an enormous body of information is available that defines the varied role of ceramide and sphingosine-1-phosphate in cell death and survival. This review specifically examines the role of ceramide and sphingosine-1- phosphate in triggering neuronal death in Alzheimer’s disease by analyzing the data from post-mortem studies and experimental research. There is compelling evidence that ceramide plays a key role in the neurodegeneration and amyloidogenesis occurring in the brain in Alzheimer’s disease. Further, it appears that ceramide and amyloid beta protein orchestrate an attack on mitochondria to set in the path-ways of cell death. However, the complexity of metabolic and signaling pathways of sphingolipid derivatives precludes an immediate identification of effective drug targets for the therapy of Alzheimer’s disease. © 2016 Bentham Science Publishers.
Reactive oxygen species, redox signaling and neuroinflammation in Alzheimer’s disease: The NF-κB connection
(Bentham Science Publishers B.V., 2015) Upinder Kaur; Priyanjalee Banerjee; Aritri Bir; Maitrayee Sinha; Atanu Biswas; Sasanka Chakrabarti
Oxidative stress and inflammatory response are important elements of Alzheimer's disease (AD) pathogenesis, but the role of redox signaling cascade and its cross-talk with inflammatory mediators have not been elucidated in details in this disorder. The review summarizes the facts about redox-signaling cascade in the cells operating through an array of kinases, phosphatases and transcription factors and their downstream components. The biology of NF-κB and its activation by reactive oxygen species (ROS) and proinflammatory cytokines in the pathogenesis of AD have been specially highlighted citing evidence both from post-mortem studies in AD brain and experimental research in animal or cell-based models of AD. The possibility of identifying new disease-modifying drugs for AD targeting NF-κBsignaling cascade has been discussed in the end. © 2015 Bentham Science Publishers.