The institute seminar on Wednesday April 25th will be held by Magnar Bjørås from Institute of Medical Microbiology, OUS-Rikshospitalet.
Title of his talk: DNA repair deficiency in neurodegenerationi
Time and place: 12.00, Auditorium, new research building, Montebello.
Accumulation of oxidative DNA damage has been proposed as a potential cause of age-related cognitive decline. The major pathway for removal of oxidative DNA base lesions is Base Excision Repair (BER), which is initiated by DNA glycosylases. In mammalian cells, at least six different DNA glycosylases remove a broad spectrum of oxidative DNA lesions. Adult neurogenesis is crucial for maintenance of hippocampus-dependent functions involved in behavior. Herein, behavioural studies of Neil DNA glycosylase deficient mice revealed significant differences in learning, memory and anxiety-like behavior. By example, neural stem/progenitor cells from Neil3 deficient mice showed impaired proliferative capacity. Further, hippocampal neurons in adult Neil3-/- mice displayed synaptic irregularities. It appears that BER of oxidative DNA damage in neural cells is required for maintenance of induced and adult neurogenesis to counteract the age associated deterioration of cognitive performance.