Animal Models for the Study of Neurological Diseases and Their Link to Sleep
Abstract
Sleep is a vital biological function governed by neuronal networks in the brainstem, hypothalamus, and thalamus. Disruptions in these circuits contribute to the sleep disturbances observed in neurodegenerative disorders, including Parkinson's disease, epilepsy, Huntington's disease, and Alzheimer's disease. Oxidative stress, mitochondrial dysfunction, neuroinflammation, and abnormal protein accumulation adversely affect sleep architecture in these conditions. The interaction among these pathological processes is believed to modify sleep-regulating circuits, consequently worsening clinical symptoms. This review examines the cellular and molecular mechanisms that impair sleep regulation in experimental models of these four disorders, emphasizing how oxidative stress, neuroinflammation and synaptic dysfunction contribute to sleep fragmentation and alterations in rapid eye movement (REM) sleep and slow-wave sleep (SWS) phases. In Parkinson's disease models (6-OHDA and MPTP), dopaminergic degeneration and damage to sleep-regulating nuclei result in daytime somnolence and disrupted sleep patterns. Epilepsy models (kainate, pentylenetetrazole, and kindling) provoke hyperexcitability and oxidative damage, compromising both REM and SWS. Huntington's disease models (R6/2 and 3-NP) demonstrate reduced sleep duration, circadian irregularities, and oxidative damage in the hypothalamus and suprachiasmatic nucleus. In Alzheimer's disease (AD) models (APP/PS1, 3xTg-AD, and Tg2576), early…
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