Deficient DNA base-excision repair in the forebrain leads to a sex-specific anxiety-like phenotype in mice.

ABSTRACT:

Background

Neuropsychiatric disorders, such as schizophrenia (SZ) and autism spectrum disorder (ASD), are common, multi-factorial and multi-symptomatic disorders. Ample evidence implicates oxidative stress, deficient repair of oxidative DNA lesions and DNA damage in the development of these disorders. However, it remains unclear whether insufficient DNA repair and resulting DNA damage are causally connected to their aetiopathology, or if increased levels of DNA damage observed in patient tissues merely accumulate as a consequence of cellular dysfunction. To assess a potential causal role for deficient DNA repair in the development of these disorders, we behaviourally characterized a mouse model in which CaMKIIa-Cre-driven postnatal conditional knockout (KO) of the core base-excisio

SUBMITTER: Mueller FS 

PROVIDER: S-EPMC9339204 | biostudies-literature | 2022 Jul

REPOSITORIES: biostudies-literature