The endocannabinoid system (ECS) is constituted by several elements, including cell membrane receptors (CB1, CB2, TRPV1, GPR55), endogenous ligands (called “endocannabinoids”, such as anandamide, AEA, and 2-araquidonylglycerol, 2-AG) and exogenous (such as delta-9-tetrahydrocannabinol, cannabidiol, and others), as well as the enzymatic machinery of synthesis and degradation of these ligands (such as fatty acid amide hydrolase, FAAH, which degrades AEA, and monoglyceride lipase, MGL, which degrades 2-AG). 

 Neuroinflammation is a key condition in many neurodegenerative processes, including Alzheimer’s disease (AD). The neuroinflammatory reaction in this disease is caused by the formation of amyloid beta peptide (Aβ) 1-42 and 1-40 oligomers and their deposition in the form of neuritic plaques in the brain parenchyma. These pathological structures, together with the formation of neurofibrillary tangles of hyperphosphorylated tau protein, constitute the main features of AD. Nowadays, SEC is generally considered to be appreciated as part of the endogenous neuroprotective mechanisms available to the CNS and is postulated as a possible target for the treatment of neuroinflammation. 

 Our research group focuses on two main lines: on the one hand, on the effect derived from the inactivation of the FAAH enzyme and, on the other hand, on the role of the cannabinoid CB2 receptor in neuroinflammatory processes in the context of AD. For this purpose, we use in vivo multiphoton microscopy, molecular biology and behavioral techniques, which allow us to approach these studies in a multidisciplinary manner.