Excess betaCTF, not Abeta: the culprit in Alzheimer-related endocytic dysfunction.
Griffin
W Sue T
WS
Donald W. Reynolds Department of Geriatrics and Institute on Aging, University of Arkansas for Medical Sciences, and the GRECC at the Central Arkansas Veterans Healthcare System, Little Rock, AR 72205, USA. griffinsuet@uams.edu
D000544:Alzheimer Disease / Q000150:complications / Q000188:drug therapy / Q000235:genetics / Q000378:metabolism*; D053829:Amyloid Precursor Protein Secretases / Q000235:genetics / Q000378:metabolism*; D016229:Amyloid beta-Peptides / Q000378:metabolism; D016564:Amyloid beta-Protein Precursor / Q000378:metabolism*; D016282:Aspartic Acid Endopeptidases / Q000235:genetics / Q000378:metabolism*; D004314:Down Syndrome / Q000150:complications / Q000235:genetics / Q000378:metabolism; D011992:Endosomes / Q000378:metabolism*; D006801:Humans; D010446:Peptide Fragments / Q000378:metabolism*
D016229:Amyloid beta-Peptides; D016564:Amyloid beta-Protein Precursor; D010446:Peptide Fragments; D053829:Amyloid Precursor Protein Secretases; D016282:Aspartic Acid Endopeptidases; C509280:BACE1 protein, human