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P4‐007: NICASTRIN IS REQUIRED FOR ZEBRAFISH PIGMENT AND BRAIN DEVELOPMENT
Author(s) -
Chong ShangWei,
Jiang YunJin,
Tang ChinHao,
You MaySu
Publication year - 2014
Publication title -
alzheimer's and dementia
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 6.713
H-Index - 118
eISSN - 1552-5279
pISSN - 1552-5260
DOI - 10.1016/j.jalz.2014.05.1521
Subject(s) - nicastrin , presenilin , amyloid precursor protein , zebrafish , biology , mutant , phenotype , microbiology and biotechnology , alzheimer's disease , notch signaling pathway , genetics , pathology , gene , medicine , signal transduction , disease
[[abstract]]Background: Alzheimer's disease (AD) is the most common form of dementia and neuropathologically characterized by the presence of neurofibrillary tangles and the deposition of β-amyloid (Aβ) in neuritic plagues. So far three genes have been identified that, when mutated, cause early onset AD: Amyloid precursor protein (APP), Presenilin-1 (PS1), and Presenilin-2 (PS2). Nicastrin is a transmembrane glycoprotein whose mutation causes a type of familial Alzheimer's disease (FAD). This protein forms gamma-secretase complex with PS1, PS2, APH-1, PEN-2 and catenins, which is involved in proteolytically processing APP to the short AD-associated peptide β-amyloid. Another well-known substrate of gamma-secretase is Notch. It has been shown that mouse Nicastrin deficiency causes neurodegeneration recently