MELATONIN AND CANNABINOIDS: MITOCHONDRIA-TARGETED MOLECULES THAT MAY REDUCE INFLAMMAGING IN NEURODEGENERATIVE DISEASES

FERES MOCAYAR; GARCÍA SEBASTIÁN; RUSSEL REITER; GARCÍA SEBASTIÁN; RUSSEL REITER; VIRNA MARTÍN GIMENÉZ; WALTER MANUCHA; VIRNA MARTÍN GIMENÉZ; WALTER MANUCHA; FERES MOCAYAR

HISTOLOGY AND HISTOPATHOLOGY

F HERNANDEZ

Lugar: Murcia; Año: 2020 vol. 35 p. 789 - 800

0213-3911

Generally, the development and progression of neurodegenerative diseases areassociated with advancing age, so they usually diagnosed in late adulthood. A primary mechanism underlying the onset of neurodegenerative diseases is neuroinflammation. Based on this background, the concept of "neuroinflammaging" has emerged. In this deregulated neuroinflammatory process, a variety of immune cells participate, especially glial cells, proinflammatory cytokines, receptors, and subcellular organelles including mitochondria, which are mainly responsible for maintaining redox balance at the cellular level. Senescence and autophagic processes also play a crucial role in the neuroinflammatory disease associated with aging. Of particular interest, melatonin, cannabinoids, and the receptors of both molecules which are closely related, exert beneficial effects on the neuroinflammatory processes that precede the onset of neurodegenerative pathologies such as Parkinson´s and Alzheimer´s diseases. Some of these neuroprotective effects are fundamentally related to its anti-inflammatory andantioxidative actions at the mitochondrial level due to its strategic functions of this organelle. The aim of this review is to summarize the most recent advances in the study of neuroinflammation and neurodegeneration associated with age and to consider the use of new mitochondrial therapeutic targets related to the endocannabinoid system and the pineal gland.