title: Association of Plasma β-Amyloid with Cognitive Performance and Decline in Chronic Kidney Disease.
abstract: Decreased β-amyloid (Aβ) clearance from the brain has been suggested to contribute to cerebral Aβ accumulation in Alzheimer's disease. Based on the idea of a dynamic Aβ equilibrium in different body compartments, plasma Aβ levels have been investigated as biomarker candidates for preclinical Alzheimer's pathology, yet with inconsistent results. Since the kidneys are involved in Aβ elimination from the blood, we evaluated how chronic kidney disease (CKD) affects the association between plasma Aβ and cognitive deficits and cognitive decline. In 28 CKD patients, stages 3-5D, and 26 control subjects with comparable vascular risk profile from the New Tools for the Prevention of Cardiovascular Disease in Chronic Kidney Disease (NTCVD) cohort, plasma total Aβ was determined with a highly sensitive electrochemiluminescence immunoassay. Cognition was evaluated using a comprehensive battery of ten neuropsychological tests at baseline and 2-year follow-up. Subjects with high plasma Aβ level (above median) demonstrated a significantly worse baseline cognitive performance than subjects exhibiting low Aβ level (summary score of global cognitive performance at baseline z = -0.46 ± 0.76 vs z = -0.08 ± 0.57, p = 0.045). Cognitive performance moderately decreased over the 2-year follow-up in subjects with high plasma Aβ level (Δz = -0.13 ± 0.51), but increased in subjects with low plasma Aβ level (Δz = 0.16 ± 0.41, p = 0.023). In linear regression analyses, baseline plasma Aβ was significantly associated with cognitive decline both in unadjusted analyses (β = -0.28, 95% CI = -0.55 to -0.01) and analyses adjusted for age (β = -0.27, 95% CI = -0.54 to -0.01). Our results suggest the utility of plasma Aβ level in predicting cognitive decline in patients suffering from CKD.
authors: Department of Neurology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Janine
authors: J
authors: Gronewold
authors: Department of Neurology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Olga
authors: O
authors: Todica
authors: Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, von-Siebold-Straße 5, 37075, Goettingen, Germany.
authors: Hans-Wolfgang
authors: HW
authors: Klafki
authors: Department of Neurology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Ulla K
authors: UK
authors: Seidel
authors: Department of Neurology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Britta
authors: B
authors: Kaltwasser
authors: Department of Psychiatry and Psychotherapy, University Medical Center Goettingen, von-Siebold-Straße 5, 37075, Goettingen, Germany.
authors: Jens
authors: J
authors: Wiltfang
authors: Department of Nephrology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Andreas
authors: A
authors: Kribben
authors: Department of Nephrology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany.
authors: Heike
authors: H
authors: Bruck
authors: Department of Neurology, University Hospital Essen, Hufelandstraße 55, 45122, Essen, Germany. dirk.hermann@uk-essen.de.
authors: Dirk M
authors: DM
authors: Hermann
mesh_terms: D000368:Aged; D016229:Amyloid beta-Peptides / Q000097:blood*; D015415:Biomarkers / Q000097:blood; D060825:Cognitive Dysfunction / Q000097:blood* / Q000175:diagnosis* / Q000503:physiopathology; D005260:Female; D005500:Follow-Up Studies; D005919:Glomerular Filtration Rate / Q000502:physiology; D006801:Humans; D008297:Male; D008875:Middle Aged; D011446:Prospective Studies; D011597:Psychomotor Performance / Q000502:physiology*; D051436:Renal Insufficiency, Chronic / Q000097:blood* / Q000175:diagnosis* / Q000503:physiopathology
chemical_list: D016229:Amyloid beta-Peptides; D015415:Biomarkers
keywords: Alzheimer’s disease; Cognitive deficits; Neurovascular hypothesis; Peripheral sink hypothesis; Vascular risk factor