AI Article Synopsis
- - Emerging research suggests cannabinoids, particularly cannabidiol (CBD), could help treat Alzheimer's disease (AD) by improving cognitive function and reducing β-amyloid pathology in mouse models.
- - The primary mechanism of action for CBD appears to involve enhancing the function of inhibitory glycine receptors (GlyR) in the hippocampus, which helps reduce neuronal hyperactivity linked to AD.
- - Disruption of the GlyR's function or CBD's ability to bind to it significantly diminishes its positive effects, indicating that targeting GlyR could be a key strategy in developing AD treatments.
Article Abstract
Emerging evidence supports the therapeutic potential of cannabinoids in Alzheimer's disease (AD), but the underlying mechanism upon how cannabinoids impact brain cognition and AD pathology remains unclear. Here we show that chronic cannabidiol (CBD) administration significantly mitigates cognitive deficiency and hippocampal β-amyloid (Aβ) pathology in 5×FAD mouse model of AD. CBD achieves its curative effect mainly through potentiating the function of inhibitory extrasynaptic glycine receptor (GlyR) in hippocampal dentate gyrus (DG). Based on the in vitro and in vivo electrophysiological recording and calcium imaging, CBD mediated anti-AD effects via GlyR are mainly accomplished by decreasing neuronal hyperactivity of granule cells in the DG of AD mice. Furthermore, the AAV-mediated ablation of DG GlyRα1, or the GlyRα1 mutation that exclusively disrupts CBD binding, significantly intercepts the anti-AD effect of CBD. These findings suggest a GlyR dependent mechanism underlying the therapeutic potential of CBD in the treatment of AD.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1038/s41380-024-02789-x | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Want AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!