Middle-aged human apoE4 targeted-replacement mice show retention deficits on a wide range of spatial memory tasks.

Apolipoprotein (apo) E4, one of three human apoE (h-apoE) isoforms, has been identified as a major genetic risk factor for Alzheimer's disease and for cognitive deficits associated with aging. However, the biological mechanisms involving apoE in learning and memory processes are unclear. A potential isoform-dependent role of apoE in cognitive processes was studied in human apoE targeted-replacement (TR) mice.

Human apoE targeted replacement mouse lines: h-apoE4 and h-apoE3 mice differ on spatial memory performance and avoidance behavior.

Apolipoprotein E4 (apoE4), one of the three most common human apoE (h-apoE) isoforms, is a major genetic risk factor for Alzheimer's disease and for cognitive deficits associated with aging. The biological mechanisms involving apoE in learning and memory processes are unclear. A potential isoform-dependent effect of h-apoE on cognitive performance was studied in gene-targeted mice, which show physiological expression levels and distribution of h-apoE3 or h-apoE4.

Increased corticosterone secretion and early-onset of cognitive decline in female apolipoprotein E-knockout mice.

In the present study, the interaction of age and apolipoprotein E (apoE)-genetic background on cognitive abilities was investigated in young (5-6 months) and aged (14-16 months) female apolipoprotein E-knockout (apoE0/0) and wild-type mice. Cognitive abilities are known to be affected by the steroid hormones corticosterone and estrogen. Therefore, we measured the activity and reactivity of the hypothalamic-pituitary-adrenal (HPA) axis expressed by circadian corticosterone concentrations and responses to novelty and controlled the regularity of the estrous cycle.

Gene x environment interaction and cognitive performance: animal studies on the role of corticosterone.

A fundamental question in the neurobiology of cognition is how stress and glucocorticoids modify learning and memory processes. Why some individuals develop cognitive deficits after stress, while other individuals improve in cognitive performance under similar adverse conditions is still unresolved. To address these questions we focus on those issues.