POSTER (Image)

POSTER PRESENTATION (Video)

PRESENTER: Lorena P. Samentar

AUTHORS: Lorena P. Samentar, Pei-Pei Pan, Arnold Salazar, Adrienne S. Bugayong, Kayvon Etebar, Durin Uddin, and Nora B. Caberoy

MENTOR: Nora B. Caberoy

ABSTRACT:

Alzheimer’s disease (AD) is a progressive neurodegenerative disease that has no cure. The pathological characteristics of Alzheimer’s include the deposition of amyloid beta plaques, formation of Tau tangles, and neuroinflammation. In AD, amyloid beta is primarily removed by phagocytosis through receptors whose activation results to inflammation. As part of our strategy to develop a cure for AD, we have created a hybrid protein. Our objective is to test whether the hybrid protein that we have generated can reduce amyloid beta load and prevent disease progression in a mouse model of AD. We administered our hybrid through daily injection in the abdomen. After 30 days, we sacrificed the mice and collected the brain and the other organs for biochemical and immunohistochemical analyses. Our results show that the hybrid protein crosses the blood brain barrier and colocalizes with the microglia and MerTK receptor in the brain. Treatment of the hybrid protein reduces Aβ burden in the brain, protects the nerve cells from dying, reduces the level of IL-6 pro-inflammatory cytokine, and is not toxic to the liver and kidneys of female 3xTg-AD mice.