Sleep deprivation aggravated amyloid β oligomers-induced damage to the cerebellum of rats: Evidence from magnetic resonance imaging
Wensheng Guo,
Xin Mao,
Ding Han,
Hongqi Wang,
Wanning Zhang,
Guitao Zhang,
Ning Zhang,
Binbin Nie,
Hui Li,
Yizhi Song,
Yan Wu,
Lirong Chang
Affiliations
Wensheng Guo
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Xin Mao
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Ding Han
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Hongqi Wang
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Wanning Zhang
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Guitao Zhang
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Ning Zhang
Department of Neuropsychiatry and Behavioral Neurology and Clinical Psychology, China National Clinical Research Center for Neurological Diseases, Beijing Tiantan Hospital, Capital Medical University, Beijing, China
Binbin Nie
Beijing Engineering Research Center of Radiographic Techniques and Equipment, Institute of High Energy Physics, Chinese Academy of Sciences, Beijing, China
Hui Li
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Yizhi Song
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China
Yan Wu
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China; Corresponding authors.
Lirong Chang
Department of Anatomy, School of Basic Medical Sciences, Beijing Key Laboratory of Neural Regeneration and Repair, Beijing Institute of Brain Disorders, Capital Medical University, Beijing, China; Corresponding authors.
For quite a long time, researches on Alzheimer's disease (AD) primarily focused on the cortex and hippocampus, while the cerebellum has been ignored because of its abnormalities considered to appear in the late stage of AD. In recent years, increasing evidence suggest that the cerebellar pathological changes possibly occur in the preclinical phase of AD, which is also associated with sleep disorder. Sleep disturbance is a high risk factor of AD. However, the changes and roles of cerebellum has rarely been reported under conditions of AD accompanied with sleep disorders. In this study, using an amyloid-β oligomers (AβO)-induced rat model of AD subjected to sleep deprivation, combining with a 7.0 T animals structural magnetic resonance imaging (MRI), we assessed structural changes of cerebellum in MRI. Our results showed that sleep deprivation combined with AβO led to an increased FA value in the anterior lobe of cerebellum, decreased ADC value in the cerebellar lobes and cerebellar nuclei, and increased cerebellum volume. Besides that, sleep deprivation exacerbated the damage of AβO to the cerebellar structural network. This study demonstrated that sleep deprivation could aggravate the damage to cerebellum induced by AβO. The present findings provide supporting evidence for the involvement of cerebellum in the early pathology of AD and sleep loss. Our data would contribute to advancing the understanding of the mysterious role of cerebellum in AD and sleep disorders, as well as would be helpful for developing non-invasive MRI biomarkers for screening early AD patients with self-reported sleep disturbances.
