Microglial Endocannabinoid Signalling in AD.
Lucia ScipioniFrancesca CiaramellanoVeronica CarnicelliAlessandro LeutiAnna Rita LizziNoemi De DominicisSergio OddiMauro MaccarronePublished in: Cells (2022)
Chronic inflammation in Alzheimer's disease (AD) has been recently identified as a major contributor to disease pathogenesis. Once activated, microglial cells, which are brain-resident immune cells, exert several key actions, including phagocytosis, chemotaxis, and the release of pro- or anti-inflammatory mediators, which could have opposite effects on brain homeostasis, depending on the stage of disease and the particular phenotype of microglial cells. The endocannabinoids (eCBs) are pleiotropic bioactive lipids increasingly recognized for their essential roles in regulating microglial activity both under normal and AD-driven pathological conditions. Here, we review the current literature regarding the involvement of this signalling system in modulating microglial phenotypes and activity in the context of homeostasis and AD-related neurodegeneration.
Keyphrases
- inflammatory response
- lipopolysaccharide induced
- lps induced
- induced apoptosis
- neuropathic pain
- anti inflammatory
- cell cycle arrest
- oxidative stress
- systematic review
- signaling pathway
- resting state
- spinal cord
- spinal cord injury
- brain injury
- cognitive decline
- functional connectivity
- pi k akt
- cerebral ischemia
- multiple sclerosis
- subarachnoid hemorrhage