Role of Lunasin in Alzheimer’s disease
Alzheimer’s disease (AD), a common form of dementia and age related progressive neurodegenerative disorder, manifests as memory loss and reduced cognitive ability. One of the hallmarks of AD is the formation of the Amyloid-beta 42 (hereafter Aβ42) plaques, which triggers oxidative stress due to aberrant signaling and finally results in the death of neurons. However, the exact mechanism causing cell death is still not well understood. We misexpressed high levels of human Aβ42 protein in the developing fly retina, which mimics AD-like neuropathology. Recently, we found that a plant protein Lunasin can ameliorate Aβ42 mediated neurodegeneration in the eye by blocking c-Jun N-terminal kinase (JNK) signaling pathway. It is known that Immune deficiency (IMD) pathway, Nuclear factor-κB (NF-κB) signaling pathway, Toll receptor pathway and JNK pathway crosstalk with each other in neurodegeneration. Here we test the role of IMD and NF-κB pathway in Aβ42 mediated neurodegeneration. Loss of function of Relish (Rel), a member of and NF-κB and its downstream gene- Diptericin rescues the small glazy eye phenotype. Our working model is that Lunasin might down-regulate JNK signalling pathway which in turn downregulates IMD pathway to ameliorate Aβ42 mediated neurodegeneration.
Primary Advisor's Department
Stander Symposium poster
"Role of Lunasin in Alzheimer’s disease" (2019). Stander Symposium Posters. 1538.