DNA base excision repair activities in mouse models of Alzheimer's disease.
Alzheimer's disease (AD) has been correlated with elevated levels of oxidative DNA damage. Base excision repair (BER) is the main repair pathway for the removal of oxidative DNA base modifications. We have recently found significant functional deficiencies in BER in brains of sporadic AD and amnestic mild cognitive impairment patients. In this study we tested whether altered BER activities are associated with appearance of symptoms in different brain regions of pre-symptomatic and symptomatic mice harboring mutant APP alone or in combination with Tau and PS1. Our results suggest that unlike in humans, the development of AD-like pathology in the studied mouse models is not associated with deficiencies in BER.
Weissman
Lior
L
Laboratory of Molecular Gerontology, National Institute on Aging, NIH, 5600 Nathan Shock Drive, Baltimore, MD 21224, USA.
de Souza-Pinto
Nadja C
NC
Mattson
Mark P
MP
Bohr
Vilhelm A
VA
D000375:Aging; D000544:Alzheimer Disease / Q000235:genetics* / Q000473:pathology*; D016564:Amyloid beta-Protein Precursor / Q000235:genetics; D000818:Animals; D001921:Brain / Q000473:pathology*; D004247:DNA; D004260:DNA Repair; D004195:Disease Models, Animal; D008297:Male; D051379:Mice; D008810:Mice, Inbred C57BL; D008822:Mice, Transgenic; D009154:Mutation; D053764:Presenilin-1 / Q000235:genetics; D058255:Protease Nexins; D011956:Receptors, Cell Surface / Q000235:genetics; D016875:tau Proteins / Q000235:genetics
C545487:APP protein, human; D016564:Amyloid beta-Protein Precursor; C054369:MAPT protein, human; C508853:PSEN1 protein, human; D053764:Presenilin-1; D058255:Protease Nexins; D011956:Receptors, Cell Surface; D016875:tau Proteins; D004247:DNA