Neuropsychiatric Inventory-Assessed Nighttime Behavior Accompanies, but Does Not Precede, Progressive Cognitive Decline Independent of Alzheimer’s Disease Histopathology
Affiliations: [a] Keenan Research Centre for Biomedical Research, the Li Ka Shing Knowledge Institute, St. Michael’s Hospital, Toronto, Canada
| [b] Department of Laboratory Medicine and Pathobiology, University of Toronto, Toronto, Canada
| [c] Division of Pathology, St. Michael’s Hospital, Toronto, Canada
| [d] Institute of Medical Sciences, University of Toronto, Toronto, Canada
| [e] Institute of Biomaterials and Biomedical Engineering, University of Toronto, Toronto, Canada
| [f] Department of Surgery, Division of Neurosurgery, Faculty of Medicine, University of Toronto, Toronto, Canada
| [g] Division of Neurosurgery, St. Michael’s Hospital, Toronto, Canada
| [h] Department of Psychiatry, Faculty of Medicine, University of Toronto, Toronto, Canada
Correspondence:
[*]
Correspondence to: David G. Munoz, MD, Department of Laboratory Medicine, Room 2-097 CC Wing, St.
Michael’s Hospital, 30 Bond Street, Toronto, ON, Canada, M5B 1W8. Tel.: +1 416 864 5858;
E-mail: [email protected].
Abstract: Background:The relationship between sleep, neuropathology, and clinical manifestations of Alzheimer’s disease (AD) remains controversial. Objective:To determine whether nighttime behaviors (NTB) are associated with the development of AD histopathology or cognitive decline. Methods:We compared NTB prevalence in subjects with or without AD lesions, and with or without progressive cognitive decline. Subjects with either absent or severe plaques and tangles were identified from the National Alzheimer’s Disease Coordinating Center data sets and classified as cognitively declining if the standard deviation from their individual mean Mini-Mental Status Examination score was ≥2, and stable if <2 regardless of their initial score. NTB was assessed using the Neuropsychiatric Inventory Questionnaire Quick Version (NPI-Q). Results:NTB was significantly greater in decliners than stable subjects in the group with severe histopathology as determined by frequent plaques (p = 0.003) or high Braak stage (p = 0.002). A similar significant trend was observed in subjects with absent plaques (p = 0.019) or tangles (p = 0.006). The prevalence of NTB was comparable between stable AD and non-AD subjects. NTB severity scores showed a similar pattern. Conclusion:The development of NTB as assessed by NPI-Q in subjects with or without AD lesions occurred concurrently with cognitive decline. Among cognitively stable subjects, the presence of AD histopathology did not alter NTB prevalence. Thus, NTB disruptions at the gross granularity level assessed by NPI-Q were much more closely related to cognitive decline than the formation of pathological lesions. Factors other than AD histopathology may mediate the association between NTB and cognitive decline.
