Rapid eye movement sleep loss associated cytomorphometric changes and neurodegeneration

Abstract

Rapid eye movement sleep (REMS) is essential for leading normal healthy living at least in higher-order mammals, including humans. In this review, we briefly survey the available literature for evidence linking cytomorphometric changes in the brain due to loss of REMS. As a mechanism of action, we add evidence that REMS loss elevates noradrenaline (NA) levels in the brain, which affects neuronal cytomorphology. These changes may be a compensatory mechanism as the changes return to normal after the subjects recover from the loss of REMS or if during REMS deprivation, the subjects are treated with NA-adrenoceptor antagonist prazosin (PRZ). We had proposed earlier that one of the fundamental functions of REMS is to maintain the level of NA in the brain. We elaborate on this idea to propose that if REMS loss continues without recovery, the sustained level of NA breaks down neurophysiologically active compensatory mechanism/s starting with changes in the neuronal cytomorphology, followed by their degeneration, leading to acute and chronic pathological conditions. Identification of neuronal cytomorphological changes could prove to be of significance for predicting future neuronal (brain) damage as well as an indicator for REMS health. Although current brain imaging techniques may not enable us to visualize changes in neuronal cytomorphology, given the rapid technological progress including use of artificial intelligence, we are optimistic that it may be a reality soon. Finally, we propose that maintenance of optimum REMS must be considered a criterion for leading a healthy life.

Keywords: Cytomorphometic changes; Karyoplasmic ratio; Neurodegeneration; Neuronal plasticity; Noradrenaline; REM sleep loss.