Cannabinerol Prevents Endoplasmic Reticulum and Mitochondria Dysfunctions in an In Vitro Model of Alzheimer’s Disease: A Network-Based Transcriptomic Analysis

pubmed logo

“Neurodegenerative disorders are affecting millions of people worldwide, impacting the healthcare system of our society. Among them, Alzheimer’s disease (AD) is the most common form of dementia, characterized by severe cognitive impairments. Neuropathological hallmarks of AD are β-amyloid (Aβ) plaques and neurofibrillary tangles, as well as endoplasmic reticulum and mitochondria dysfunctions, which finally lead to apoptosis and neuronal loss.

Since, to date, there is no definitive cure, new therapeutic and prevention strategies are of crucial importance. In this scenario, cannabinoids are deeply investigated as promising neuroprotective compounds for AD. In this study, we evaluated the potential neuroprotective role of cannabinerol (CBNR) in an in vitro cellular model of AD via next-generation sequencing.

We observed that CBNR pretreatment counteracts the Aβ-induced loss of cell viability of differentiated SH-SY5Y cells. Moreover, a network-based transcriptomic analysis revealed that CBNR restores normal mitochondrial and endoplasmic reticulum functions in the AD model. Specifically, the most important genes regulated by CBNR are related mainly to oxidative phosphorylation (COX6B1OXA1LMT-CO2MT-CO3), protein folding (HSPA5) and degradation (CUL3FBXW7UBE2D1), and glucose (G6PC3) and lipid (HSD17B7ERG28SCD) metabolism.

Therefore, these results suggest that CBNR could be a new neuroprotective agent helpful in the prevention of AD dysfunctions.”

https://pubmed.ncbi.nlm.nih.gov/38920643/

“In conclusion, our study demonstrates that the phytocannabinoid CBNR displays neuroprotective properties in an Aβ-induced AD model in differentiated SH-SY5Y cells. Indeed, it restores mitochondrial and endoplasmic reticulum dysfunctions, regulating genes related to oxidative phosphorylation, protein folding, ubiquitin-mediated degradation, and glucose and lipid metabolism. Therefore, CBNR could be a novel molecule able to prevent some of the key early features of AD and potentially other diseases characterized by similar dysfunctions.”

https://www.mdpi.com/2073-4409/13/12/1012

Leave a Reply

Your email address will not be published. Required fields are marked *