Orexin A peptidergic system: comparative sleep behavior, morphology and population in brains between wild type and Alzheimer’s disease mice

Sleep disturbance is common in patients with Alzheimer’s disease (AD), and orexin A is a pivotal neurotransmitter for bidirectionally regulating the amyloid-β (Aβ) deposition of AD brain and poor sleep. In the present study, we examined the characteristic of sleep–wake architecture in APPswe/PSldE9...

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Published in:Brain Structure and Function 2022-04, Vol.227 (3), p.1051-1065
Main Authors: Zhao, Peng, You, Yaqian, Wang, Zhe, Zhou, Yanjun, Chai, Gaoshang, Yan, Gen, Jin, Zhewu, Wang, Qing, Sun, Hongxu
Format: Article
Language:English
Subjects:
Alzheimer Disease - metabolism
Alzheimer's disease
Amyloid beta-Peptides - metabolism
Amyloid beta-Protein Precursor - genetics
Amyloid beta-Protein Precursor - metabolism
Animals
Biomedical and Life Sciences
Biomedicine
Brain - metabolism
Cell Biology
Disease Models, Animal
EEG
Electromyography
Humans
Mice
Mice, Transgenic
Morphology
Neurodegenerative diseases
Neurology
Neurosciences
NREM sleep
Orexins
Orexins - metabolism
Original
Original Article
Presenilin 1
Presenilin-1 - genetics
Presenilin-1 - metabolism
Sleep
Sleep and wakefulness
β-Amyloid
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Summary:Sleep disturbance is common in patients with Alzheimer’s disease (AD), and orexin A is a pivotal neurotransmitter for bidirectionally regulating the amyloid-β (Aβ) deposition of AD brain and poor sleep. In the present study, we examined the characteristic of sleep–wake architecture in APPswe/PSldE9 (APP/PS1) and Aβ-treated mice using electroencephalogram (EEG) and electromyographic (EMG) analysis. We compared the expression of orexin A, distribution, and morphology of the corresponding orexin A-positive neurons using innovative methods including three-dimensional reconstruction and brain tissue clearing between wild type (WT) and APP/PS1 mice. Results from our study demonstrated that increased wakefulness and reduced NREM sleep were seen in APP/PS1 and Aβ treated mice, while the expression of orexin A was significantly upregulated. Higher density and distribution of orexin A-positive neurons were seen in APP/PS1 mice, with a location of 1.06 mm–2.30 mm away from the anterior fontanelle compared to 1.34 mm–2.18 mm away from the anterior fontanelle in WT mice. These results suggested that the population and distribution of orexin A may play an important role in the progression of AD.
ISSN:1863-2653
1863-2661
0340-2061
DOI:10.1007/s00429-021-02447-w