Total body 100-mGy X-irradiation does not induce Alzheimer's disease-like pathogenesis or memory impairment in mice

The cause and progression of alzheimer's disease (ad) are poorly understood. possible cognitive and behavioral consequences induced by low-dose radiation are important because humans are exposed to ionizing radiation from various sources. early transcriptional response in murine brain to low-dose x-rays (100 mgy) has been reported,suggesting alterations of molecular networks and pathways associated with cognitive functions,advanced aging and ad. to investigate acute and late transcriptional,pathological and cognitive consequences of low-dose radiation,we applied an acute dose of 100-mgy total body irradiation (tbi) with x-rays to c57bl/6j jms mice. we collected hippocampi and analyzed expression of 84 ad-related genes. mouse learning ability and memory were assessed with the morris water maze test. we performed in vivo pet scans with 11c-pib,a radiolabeled ligand for amyloid imaging,to detect fibrillary amyloid beta peptide (aβ) accumulation,and examined characteristic ad pathologies with immunohistochemical staining of amyloid precursor protein (app),aβ,tau and phosphorylated tau (p-tau). mrna studies showed significant downregulation of only two of 84 ad-related genes,apbb1 and lrp1,at 4 h after irradiation,and of only one gene,il1α,at 1 year after irradiation. spatial learning ability and memory were not significantly affected at 1 or 2 years after irradiation. no induction of amyloid fibrillogenesis or changes in app,aβ,tau,or p-tau expression was detected at 4 months or 2 years after irradiation. tbi induced early or late transcriptional alteration in only a few ad-related genes but did not significantly affect spatial learning,memory or ad-like pathological change in mice. © 2013 the author.