Affiliations: [a]
Banner Alzheimer’s Institute, Phoenix, AZ, USA
| [b] Department of Neurobiology, Barrow Neurological Institute, Phoenix, AZ, USA
Correspondence:
[*]
Correspondence to: Elliott Mufson, PhD, Director, Alzheimer’s Disease Research Laboratory, Professor, Department of Neurobiology, Barrow Neurological Institute, 350 W. Thomas Rd., Phoenix, AZ 85013, USA. Tel.: +1 602 406 8525; Fax: +1 602 406 8520; E-mail: elliott.mufson@dignityhealth.org.
Abstract: The aim of this study was to determine the interaction between cerebral amyloid angiopathy (CAA) and Braak staging on cognition in the elderly. The study used a total of 141 subjects consisting of 72 non-cognitively impaired (NCI), 33 mild cognitive impairment (MCI), 36 Alzheimer’s disease (AD) cases displaying Braak stages 0-II and III from the Rush Religious Order Study cohort. The association between Braak stage and CAA status and cognition was evaluated using a series of regression models that adjusted for age at death, sex, education, APOE ɛ4 status, and Consortium to Establish a Registry for Alzheimer’s Disease (CERAD) neuropathological diagnosis. Individuals with CAA were more likely to be classified as Braak stage III relative to those without CAA [OR = 2.33, 95% CI (1.06, 5.14), p = 0.04]. A significant interaction was found between Braak stage and CAA status on a global cognitive score (β = –0.58, SE = 0.25, p = 0.02). Episodic memory also showed a significant association between Braak stage and CAA (β= –0.75, SE = 0.35, p = 0.03). These data suggest that there is a significant interaction between tau pathology and cerebrovascular lesions on cognition within the AD clinical spectrum.
