Accelerated reduction of serum thyroxine and hippocampal histone acetylation links to exacerbation of spatial memory impairment in aged CD-1 mice pubertally exposed to bisphenol-a.

Age-related cognitive decline has been associated with changes in endogenous hormones and epigenetic modification of chromatin, including histone acetylation. Developmental exposure to endocrine disrupting chemicals, such as bisphenol-A (BPA) that produces endocrine disruption and epigenetic changes, may be a risk factor for accelerating cognitive deficits during aging. Thus, we exposed CD-1 mice to BPA (0, 1, and 100 mg/l BPA in the drinking water) orally during puberty (from postnatal days 28 to 56) and investigated whether pubertal BPA exposure exacerbates the age-related impairment of spatial cognition in old age (18 months old) and whether serum sex and thyroid hormones or hippocampal histone acetylation (H3K9ac and H4K8ac) are associated with cognitive effects.

PIN1-842G/C and -667T/C polymorphisms are not associated with the susceptibility of Alzheimer's disease: pooled analysis of epidemiologic studies.

Associations between PIN1 gene polymorphisms and Alzheimer's disease (AD) risk remain controversial, possibly because single studies often lack sufficient statistical power. In this study, we performed a meta-analysis to evaluate the association of two commonly studied PIN1 polymorphisms, -842G/C and -667T/C, with the risk of AD. Relevant studies were identified from PubMed, EMBASE, and China National Knowledge Infrastructure up to October 2012.