OBJECTIVE: Normal sleep-wake regulation is dependent upon an oscillatory circadian rhythm promoting alertness and sleep at appropriate times of day. Circadian rhythms have been noted to be disturbed as a consequence of both normal aging and age-associated pathologies like Alzheimer disease (AD). However, the relationship between the consequences of normal versus pathological aging upon circadian regulation remains unclear. The authors evaluated the similarities and differences between the consequences of aging and AD on endogenous circadian rhythm. METHODS: Authors measured locomotor activity and, with a constant routine protocol, core body temperature, examining differences and similarities in circadian disturbances in groups of normal elderly and patients with probable AD (pAD), as compared with a comparison group of young, normal volunteers, measuring endogenous circadian amplitude (ECA) and endogenous circadian phase (ECP) of core body temperature, and made parametric and nonparametric assessments of locomotor activity rhythms. RESULTS: The ECP of core body temperature was delayed in patients with pAD versus both normal young and normal elderly subjects, whereas the ECA was reduced both in normal elderly and pAD subjects compared with a comparison group of young subjects. There was also disassociation of the activity and core body temperature rhythms in both age groups versus the young subjects. CONCLUSIONS: Authors observed changes in endogenous circadian rhythm in pAD that were consonant with those seen in normal aging (amplitude reduction; loss of phase coordination) and also observed changes that were apparently discrete from those seen in normal aging (phase delay).
OBJECTIVE: Normal sleep-wake regulation is dependent upon an oscillatory circadian rhythm promoting alertness and sleep at appropriate times of day. Circadian rhythms have been noted to be disturbed as a consequence of both normal aging and age-associated pathologies like Alzheimer disease (AD). However, the relationship between the consequences of normal versus pathological aging upon circadian regulation remains unclear. The authors evaluated the similarities and differences between the consequences of aging and AD on endogenous circadian rhythm. METHODS: Authors measured locomotor activity and, with a constant routine protocol, core body temperature, examining differences and similarities in circadian disturbances in groups of normal elderly and patients with probable AD (pAD), as compared with a comparison group of young, normal volunteers, measuring endogenous circadian amplitude (ECA) and endogenous circadian phase (ECP) of core body temperature, and made parametric and nonparametric assessments of locomotor activity rhythms. RESULTS: The ECP of core body temperature was delayed in patients with pAD versus both normal young and normal elderly subjects, whereas the ECA was reduced both in normal elderly and pAD subjects compared with a comparison group of young subjects. There was also disassociation of the activity and core body temperature rhythms in both age groups versus the young subjects. CONCLUSIONS: Authors observed changes in endogenous circadian rhythm in pAD that were consonant with those seen in normal aging (amplitude reduction; loss of phase coordination) and also observed changes that were apparently discrete from those seen in normal aging (phase delay).
Authors: John D Outen; M Haroon Burhanullah; Ryan Vandrey; Halima Amjad; David G Harper; Regan E Patrick; Rose L May; Marc E Agronin; Brent P Forester; Paul B Rosenberg Journal: Am J Geriatr Psychiatry Date: 2021-01-27 Impact factor: 4.105
Authors: H Batinga; A Martinez-Nicolas; M Zornoza-Moreno; M Sánchez-Solis; E Larqué; M T Mondéjar; M Moreno-Casbas; F J García; M Campos; M A Rol; J A Madrid Journal: Age (Dordr) Date: 2015-03-27
Authors: Matthew R Blake; Scott D Holbrook; Joanna Kotwica-Rolinska; Eileen S Chow; Doris Kretzschmar; Jadwiga M Giebultowicz Journal: Neurobiol Dis Date: 2015-03-10 Impact factor: 5.996
Authors: Erik S Musiek; Meghana Bhimasani; Margaret A Zangrilli; John C Morris; David M Holtzman; Yo-El S Ju Journal: JAMA Neurol Date: 2018-05-01 Impact factor: 18.302