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Lookup NU author(s): Professor Johannes Attems
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© 2016 International Society of Neuropathology While chronic kidney disease seems to be an independent risk factor for cognitive decline, its impact on cerebral amyloid-β (Aβ) depositions, one hallmark of Alzheimer's Disease (AD) pathology, has not been investigated. Utilizing 80 male nontransgenic spontaneously hypertensive stroke prone rats (SHRSP) at various ages (12 to 44 weeks), tubulointerstitial renal damage, prevalence of cerebral microhemorrhages and Aβ accumulations were quantified. Using age-adjusted general linear models we investigated the main and interaction effects of renal damage and cerebral microhemorrhages on cerebral Aβ load. In addition, using post mortem human brain tissue of 16 stroke patients we examined the co-localization of perivascular Aβ deposits and small vessel wall damage. Statistical models revealed an age-independent main effect of tubulointerstitial kidney damage on brain Aβ accumulations, which was reinforced by the consecutive presence of cerebral microhemorrhages. Moreover, cerebral microhemorrhages independently predicted brain Aβ burden in SHRSP. In up to 69% of all human cases perivascular Aβ deposits were detected in the direct vicinity of small vessel wall damage. Our results support the associations between vascular pathology and Aβ deposition, and demonstrate a relationship between chronic kidney disease and cerebral Aβ pathology. Hence, our data suggest that prevention of chronic renal damage may reduce cerebral Aβ pathology.
Author(s): Pirici D, Stanaszek L, Garz C, Niklass S, Heinze H-J, Kalinski T, Attems J, Schreiber S
Publication type: Article
Publication status: Published
Journal: Brain Pathology
Year: 2017
Volume: 27
Issue: 2
Pages: 169-180
Print publication date: 01/03/2017
Online publication date: 08/04/2016
Acceptance date: 30/03/2016
ISSN (print): 1015-6305
ISSN (electronic): 1750-3639
Publisher: Blackwell Publishing Ltd
URL: https://doi.org/10.1111/bpa.12384
DOI: 10.1111/bpa.12384
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