| Article ID | Journal | Published Year | Pages | File Type |
|---|---|---|---|---|
| 4326192 | Brain Research | 2011 | 7 Pages |
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) APPswe/PS1ΔE9 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). CB1 immunoreactivity in the CA1 and CA2/3 hippocampal regions was significantly decreased in the dtg APPswe/PS1ΔE9 mice compared to non-transgenic littermates. Reduced CB1 expression in dtg APPswe/PS1ΔE9 mice was associated with astroglial proliferation and elevated expression of the cytokines inducible nitric oxide synthase and tumor necrosis factor alpha. This finding suggests an anti-inflammatory effect of cannabinoids that is mediated by CB1 receptor, particularly in the CA2/3 region of the hippocampus. Furthermore, the study suggests a decreased CB1 receptor expression may result in diminished anti-inflammatory processes, exacerbating the neuropathology associated with Alzheimer's disease.
Research HighlightsThe significant findings were: ► Reduction of CB1-IR neurons in CA1 hippocampal region of dtg APPswe/PS1ΔE9 mice. ► Increased astrocytes in CA1 compared to CA2/3 region in dtg APPswe/PS1ΔE9 mice. ► Increased levels of iNOS and TNFα in the hippocampus of dtg APPswe/PS1ΔE9 mice.
