AI Article Synopsis
- Circadian rhythms, managed by the suprachiasmatic nucleus (the "master clock"), are influenced by light and can be disrupted by unhealthy lifestyles and chronic light disturbances, impacting neurotransmission.
- Recent research suggests a link between circadian rhythm disruptions (CRd) and Alzheimer's disease, specifically looking at how endocannabinoids might play a role in this connection through pathways involving the retino-hypothalamic tract.
- Cannabinoid receptors in the suprachiasmatic nucleus may help regulate circadian phases and show potential for improving cognitive issues by reducing tau pathology and activating microglia, indicating a possible therapeutic target for addressing CRd and Alzheimer's disease.
Article Abstract
Circadian rhythms are 24-hour natural rhythms regulated by the suprachiasmatic nucleus, also known as the "master clock". The retino-hypothalamic tract entrains suprachiasmatic nucleus with photic information to synchronise endogenous circadian rhythms with the Earth's light-dark cycle. However, despite the robustness of circadian rhythms, an unhealthy lifestyle and chronic photic disturbances cause circadian rhythm disruption in the suprachiasmatic nucleus's TTFL loops via affecting glutamate and γ-aminobutyric acid-mediated neurotransmission in the suprachiasmatic nucleus. Recently, considerable evidence has been shown correlating CRd with the incidence of Alzheimer's disease. The present review aims to identify the existence and signalling of endocannabinoids in CRd induced Alzheimer's disease through retino-hypothalamic tract- suprachiasmatic nucleus-cortex. Immunohistochemistry has confirmed the expression of cannabinoid receptor 1 in the suprachiasmatic nucleus to modulate the circadian phases of the master clock. Literature also suggests that cannabinoids may alter activity of suprachiasmatic nucleus by influencing the activity of their major neurotransmitter γ-aminobutyric acid or by interacting indirectly with the suprachiasmatic nucleus's two other major inputs i.e., the geniculo-hypothalamic tract-mediated release of neuropeptide Y and serotonergic inputs from the dorsal raphe nuclei. Besides, the expression of cannabinoid receptor 2 ameliorates cognitive deficits via reduction of tauopathy and microglial activation. In conclusion, endocannabinoids may be identified as a putative target for correcting CRd and decelerating Alzheimer's disease.
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC8729113 | PMC |
| http://dx.doi.org/10.1016/j.arr.2021.101533 | DOI Listing |
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