Abstract
INTRODUCTION
As the chemokine receptor5 (CCR5) may play a role in ischemia, we studied the links between CCR5 deficiency, the sensitivity of neurons to oxidative stress, and the development of dementia.
METHODS
Logistic regression models with CCR5/apolipoprotein E (ApoE) polymorphisms were applied on a sample of 205 cognitively normal individuals and 189 dementia patients from Geneva. The impact of oxidative stress on Ccr5 expression and cell death was assessed in mice neurons.
RESULTS
CCR5-Δ32 allele synergized with ApoEε4 as risk factor for dementia and specifically for dementia with a vascular component. We confirmed these results in an independent cohort from Italy (157 cognitively normal and 620 dementia). Carriers of the ApoEε4/CCR5-Δ32 genotype aged ≥80 years have an 11-fold greater risk of vascular-and-mixed dementia. Oxidative stress-induced cell death in Ccr5−/−
mice neurons.
DISCUSSION
We propose the vulnerability of CCR5-deficient neurons in response to oxidative stress as possible mechanisms contributing to dementia.


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This post is Copyright: Benjamin B. Tournier,
Silvia Sorce,
Antoine Marteyn,
Roberta Ghidoni,
Luisa Benussi,
Giuliano Binetti,
François R Herrmann,
Karl‐Heinz Krause,
Dina Zekry | July 25, 2023

Wiley: Alzheimer’s & Dementia: Table of Contents