Author(s): Gorman MR, Yellon S
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Abstract Using a rodent model for neuropathology induced by human amyloid precursor protein, the present study tested the hypothesis that 24 h rest/activity rhythms deteriorate with age. A lifespan of rest/activity patterns was studied in transgenic Tg2576 mice and wild-type controls. Classic indices of circadian timekeeping, including onsets, offsets, and the duration of nighttime activity, were stable throughout the 96-week study. Analyses of ultradian bout activity revealed significant genotype and age-related changes in the duration and intensity of activity bouts, as well as amplitude of the 24 h rhythm. Tg2576 mice had more total activity counts, fewer bouts/24 h, more counts/bout, and longer bout time than wild-type controls. Amyloid deposits and plaques were solely found in specific cortex regions in aged postmortem Tg2576 mice, but were not evident in the hypothalamus or suprachiasmatic nucleus; this neuropathology was absent from brains of wild-type controls. These findings suggest that amyloidosis of the Tg2576 mouse exerts little influence on timing of locomotor activity in the circadian domain but significantly alters the temporal structure of ultradian activity.
This article was published in Chronobiol Int
and referenced in Journal of Neurology & Neurophysiology