Biomedical sciences

Biomedical sciences


Host Department
Department of Biomedical Sciences



Research Topic B

Abstract of the proposed UNIPhD research project


Mutations of Presenilin 2 (PS2) associated with familial Alzheimer’s disease (FAD) lead to reduced mitochondrial Ca2+ signal and impaired ATP synthesis making neurons unable to cope with glutamate-induced excitotoxicity. Similar changes in Ca2+ dynamics are also seen in astrocytes of FAD mouse models suggesting a role of altered mitochondrial bioenergetics in the disease-related neuroinflammation. This project investigates the role of mitochondrial Ca2+ signaling and ER-mitochondria cross-talk in neuronal excitotoxicity and in driving the reactivity of astrocytes and microglia in FAD.



Short bio

I am Neha Kachappilly, a BS-MS graduate in Biology from IISER Thiruvananthapuram, India. For my Master’s research project, I studied the aggregation of alpha-synuclein, the protein associated with Parkinson’s and a few other neurodegenerative diseases. I have always been interested in research into the molecular mechanisms of neurodegenerative diseases, and am hoping to contribute towards the development of better therapeutics for handling these diseases. As a PhD student in Prof Pizzo’s group, I will work on understanding the role of mitochondrial bioenergetics in neuronal excitotoxicity and neuroinflammation associated with familial Alzheimer’s disease.

Topic assigned to
Neha Kachappilly


Project documents