Plasma amyloid-beta, Abeta1-42, load is reduced by haemodialysis.

J Alzheimers Dis

Banco de Tejidos para Investigaciones Neurológicas, Facultad de Medicina, Universidad Complutense de Madrid, and Servicio de Bioquímica, Hospital Ramón Cajal, Spain.

Published: December 2006

Patients with chronic renal failure treated with haemodialysis have vascular risk factors that, in the general population, are associated with increased prevalence of Alzheimer's disease (AD). Patients in haemodialysis, however, present different kinds of dementia but they do not have an increased risk of AD. We have hypothesized that amyloid-beta (Abeta)1-42 is washed out from plasma during the dialysis and that this procedure enhances Abeta elimination and reduces the risk of AD. We have measured plasma Abeta1-42 levels in 11 patients with renal failure, before and after haemodialysis. A single procedure reduced the plasma Abeta levels in all subjects with a mean decrement of 30% of baseline. Since Abeta deposition could be altered by certain metals like Cu and Zn, we have also measured the effects of dialysis on the levels of these ions in plasma. We found no changes in levels of Cu and Zn after dialysis. Haemodialysis, therefore, reduces very effectively plasma Abeta without modifying Cu and Zn levels. The potential use of this strategy in patients with AD requires further investigation.

Download full-text PDF

Source
http://dx.doi.org/10.3233/jad-2006-10413DOI Listing

Publication Analysis

Top Keywords

amyloid-beta abeta1-42
8
renal failure
8
plasma abeta
8
plasma
6
haemodialysis
5
levels
5
plasma amyloid-beta
4
abeta1-42 load
4
load reduced
4
reduced haemodialysis
4

Similar Publications

Introduction: Studies have shown that blood biomarkers can differentiate dementia disorders. However, the diagnosis of dementia still relies primarily on cerebrospinal fluid and imaging modalities. The new disease-modifying treatments call for more widely applicable biomarkers.

View Article and Find Full Text PDF

Background: Recent studies show that N6-methyladenosine (m6A) plays an important role in the pathogenesis of the Alzheimer's disease (AD), while the mechanisms involved were studied insufficiently.

Aims: The present study aimed to explore the effect of human insulin-like growth factor 2 (IGF2) mRNA binding proteins 2 (IGF2BP2), one of the m6A-binding proteins on the progression of AD.

Materials & Methods: The mRNA and protein expression level were determined using RT-qPCR and western blot, respectively.

View Article and Find Full Text PDF

Aging and voluntary exercise's effects on Aβ1-42 levels, endoplasmic reticulum stress factors, and apoptosis in the hippocampus of old male rats.

Brain Res

January 2025

Department of Physiology, School of Medicine, Urmia University of Medical Sciences, Urmia, Iran; Neurophysiology Research Center, Cellular and Molecular Medicine Research Institute, Urmia University of Medical Sciences, Urmia, Iran. Electronic address:

Within the aging cortex, amyloid beta peptide (Aβ) is a crucial element of the senile plaques, a hallmark feature often observed in cases of Alzheimer's disease (AD). The UPR (unfolded protein response), a cellular mechanism for protein folding, is switched on by Aβ accumulation. Endoplasmic reticulum (ER) stress has been identified as playing a role in aging and the development of neurodegenerative diseases.

View Article and Find Full Text PDF

Introduction: Previous studies have examined the predictive accuracy of plasma amyloid beta (Aβ) biomarkers in clinical cohorts. However, their accuracy for predicting amyloid-positive patients in community-based cohorts is unclear. This study aimed to determine the predictive accuracy of Aβ precursor protein 669-711/Aβ1-42, Aβ1-40/1-42 and their composite biomarkers for brain amyloid deposition or the clinical progression in community-dwelling older adults with mild cognitive impairment (MCI).

View Article and Find Full Text PDF

Background: Cold inducible RNA-binding protein (CIRP) is an important danger-associated molecular pattern involved in tissue-specific and systemic inflammation related to inflammation and Alzheimer's disease (AD). However, the precise roles and mechanism of CIRP in the functional changes in astrocytes during the development of AD are still unknown. This study aimed to assess gene expression alterations in astrocytes after they overexpress CIRP (oe-CIRP) and to explore the relationship between abnormal CIRP expression and AD.

View Article and Find Full Text PDF

Want AI Summaries of new PubMed Abstracts delivered to your In-box?

Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!