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Full-Text Articles in Life Sciences
App Regulates Microglial Phenotype In A Mouse Model Of Alzheimer's Disease, Gunjan D. Manocha, Angela M. Floden, Keiko Rausch, Joshua A. Kulas, Brett A. Mcgregor, Lalida Rojanathammanee, Kelley R. Puig, Kendra L. Puig, Sanjib Karki, Michael R. Nichols, Diane C. Darland, James E. Porter, Colin K. Combs
App Regulates Microglial Phenotype In A Mouse Model Of Alzheimer's Disease, Gunjan D. Manocha, Angela M. Floden, Keiko Rausch, Joshua A. Kulas, Brett A. Mcgregor, Lalida Rojanathammanee, Kelley R. Puig, Kendra L. Puig, Sanjib Karki, Michael R. Nichols, Diane C. Darland, James E. Porter, Colin K. Combs
Biology Faculty Publications
Prior work suggests that amyloid precursor protein (APP) can function as a proinflammatory receptor on immune cells, such as monocytes and microglia. Therefore, we hypothesized that APP serves this function in microglia during Alzheimer's disease. Although fibrillar amyloid β (Aβ)-stimulated cytokine secretion from both wild-type and APP knock-out (mAPP−/−) microglial cultures, oligomeric Aβ was unable to stimulate increased secretion from mAPP−/− cells. This was consistent with an ability of oligomeric Aβ to bind APP. Similarly, intracerebroventricular infusions of oligomeric Aβ produced less microgliosis in mAPP−/− mice compared with wild-type mice. The mAPP−/− mice crossed to an APP/PS1 transgenic mouse line …