Distribution patterns of cannabinoid CB1 receptors in the hippocampus of APPswe/PS1ΔE9 double transgenic mice.

Cannabinoids have neuroprotective effects that are exerted primarily through cannabinoid CB1 receptors in the brain. This study characterized CB1 receptor distribution in the double transgenic (dtg) APP(swe)/PS1(ΔE9) mouse model for Alzheimer's disease. Immunohistochemical labeling of CB1 protein in non-transgenic mice revealed that CB1 was highly expressed in the hippocampus, with the greatest density of CB1 protein observed in the combined hippocampal subregions CA2 and CA3 (CA2/3).

17α-estradiol attenuates neuron loss in ovariectomized Dtg AβPP/PS1 mice.

Quantitative microanalysis of brains from patients with Alzheimer's disease (AD) find neuronal loss and neuroinflammation in structures that control cognitive function. Though historically difficult to recapitulate in experimental models, several groups have recently reported that by middle-age, transgenic mice that co-express high levels of two AD-associated mutations, amyloid-β protein precursor (AβPP(swe)) and presenilin 1 (PS1(ΔE9)), undergo significant AD-type neuron loss in sub-cortical nuclei with heavy catecholaminergic projections to the hippocampal formation. Here we report that by 13 months of age these dtg AβPP(swe)/PS1(ΔE9) mice also show significant loss of pyramidal neuron in a critical region for learning and memory, the CA1 subregion of hippocampus, as a direct function of amyloid-β (Aβ) aggregation.

The role of PI 3-kinase p110beta in AKT signally, cell survival, and proliferation in human prostate cancer cells.

Background: Class IA PI 3-kinases produce phosphatidylinositol (3,4,5)-trisphosphate (PIP3). PIP3 is bound by AKT which facilities its activation by PDK1. Activated AKT promotes cell survival and stimulates cell proliferation.