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The neuropathology of Alzheimer’s Disease (AD) is a complex system of neurodegenerative factors that contribute to the loss of brain function. One of the most studied factors is the aggregation of amyloid plaques within the brain. These plaques are formed from the improper cleavage of the amyloid precursor protein (APP) to form the hydrophobic peptide, Aβ42. These peptides congregate in plaques that surround neuronal cells and inhibit their function. As the these cells begin to degrade, microglial cells that act as the central nervous system’s immune defense attempt to remove these plaques. However these cells are not capable in fully removing these plaques and incite an inflammatory response through the release of several cytokines and chemokines from the microglial cell. These messengers can induce oxidative stress within the CNS and lead to further cell damage. Our disease model is based on the visual system of the Drosophila melanogaster. The Aβ42 protein is misexpressed during the development of the photoreceptor neurons which results in observable loss of eye formation in the adult fly. We propose by introducing a known anti-inflammatory protein, Lunasin, into our disease model we can further understand the role of inflammation in AD neuropathology. Here present the findings of our studies.
Madhuri Kango-Singh, Amit Singh
Primary Advisor's Department
Stander Symposium poster
Glenn, Neil William and Sarkar, Ankita, "Neuroprotective Function of Lunasin in Alzheimer's Disease Model" (2016). Stander Symposium Posters. 804.