Lack of Association Between the CCR5-delta32 Polymorphism and Neurodegenerative Disorders.

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Abstract

Recent studies have suggested that diminished Ccr5 functioning has an effect on synaptic plasticity and hippocampal memory in mouse models. CCR5-delta32, a 32-bp frameshift deletion in human CCR5 encoding a nonfunctional receptor, has been reported to have a protective effect against human immunodeficiency virus infection but its role as a modifier of neurodegenerative disease has been minimally explored. We investigated whether the CCR5-delta32 polymorphism could have an effect in the context of human neurodegenerative diseases.

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Journal

Journal ID (iso-abbrev): Alzheimer Dis Assoc Disord

Title: Alzheimer disease and associated disorders

Publisher: Ovid Technologies (Wolters Kluwer Health)

ISSN (Electronic): 1546-4156

ISSN (Print): 0893-0341

Publication date (Electronic): January 24 2020

Volume: 34

Issue: 3

Affiliations

[1 ] Department of Psychiatry, Semel Institute for Neuroscience and Human Behavior, David Geffen School of Medicine, University of California Los Angeles, Los Angeles.

[2 ] Department of Neurology, Memory and Aging Center, University of California San Francisco, San Francisco, CA.

Article

Mid ID: NIHMS1549490 Publisher Item ID: 00002093-202007000-00009

DOI: 10.1097/WAD.0000000000000367

PMC ID: 7365743

PubMed ID: 31972607

SO-VID: b4fabc18-cec0-4916-a253-e234404437cb

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