Abstract
Transgenic modification of the two most common genes (APPsw, PS1ΔE9) related to familial Alzheimer’s disease (AD) in rats has produced a rodent model that develops pathognomonic signs of AD without genetic tau-protein modification. We used 17-month-old AD rats (n = 8) and age-matched controls (AC, n = 7) to evaluate differences in sleep behavior and EEG features during wakefulness (WAKE), non-rapid eye movement sleep (NREM), and rapid eye movement sleep (REM) over 24-h EEG recording (12:12h dark–light cycle). We discovered that AD rats had more sleep–wake transitions and an increased probability of shorter REM and NREM bouts. AD rats also expressed a more uniform distribution of the relative spectral power. Through analysis of information content in the EEG using entropy of difference, AD animals demonstrated less EEG information during WAKE, but more information during NREM. This seems to indicate a limited range of changes in EEG activity that could be caused by an AD-induced change in inhibitory network function as reflected by increased GABAAR-β2 expression but no increase in GAD-67 in AD animals. In conclusion, this transgenic rat model of Alzheimer’s disease demonstrates less obvious EEG features of WAKE during wakefulness and less canonical features of sleep during sleep.
Highlights
With an aging society, more people will suffer from neurodegenerative disorders like Alzheimer’s disease (AD) [1] and present an increasing economic burden to relatives, societies, and healthcare providers [2]
We did not observe significant differences in weight, age, and gender between the aged control (AC) (n = 7) and AD (n = 8) animals used for the sleep and EEG analyses
The chi-squared test indicated no significant differences in gender distribution (AC: 3 females, 4 males; AD: 2 females, 6 males; p = 0.906)
Summary
More people will suffer from neurodegenerative disorders like Alzheimer’s disease (AD) [1] and present an increasing economic burden to relatives, societies, and healthcare providers [2]. We focused on the sleep architecture and electroencephalographic (EEG) characteristics of different vigilance states of the TgF344-AD rat model at an early disease stage and compared the results to age-matched healthy control animals. We relate these changes with biochemical evidence of changes in the inhibitory network function. To investigate brain dynamics at early stages, the use of animal models known to develop AD confers large advantages
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