[HTML][HTML] The neuronal adaptor protein X11α reduces Aβ levels in the brains of Alzheimer's APPswe Tg2576 transgenic mice
JH Lee, KF Lau, MS Perkinton, CL Standen… - Journal of Biological …, 2003 - ASBMB
Increased production and deposition of the 40-42-amino acid β-amyloid peptide (Aβ) is
believed to be central to the pathogenesis of Alzheimer's disease. Aβ is derived from the
amyloid precursor protein (APP), but the mechanisms that regulate APP processing to
produce Aβ are not fully understood. X11α (also known as munc-18-interacting protein-1
(Mint1)) is a neuronal adaptor protein that binds APP and modulates APP processing in
transfected non-neuronal cells. To investigate the in vivo effect of X11α on Aβ production in …
believed to be central to the pathogenesis of Alzheimer's disease. Aβ is derived from the
amyloid precursor protein (APP), but the mechanisms that regulate APP processing to
produce Aβ are not fully understood. X11α (also known as munc-18-interacting protein-1
(Mint1)) is a neuronal adaptor protein that binds APP and modulates APP processing in
transfected non-neuronal cells. To investigate the in vivo effect of X11α on Aβ production in …