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The age factor in Alzheimer's disease
1Department of Molecular Neuroscience, Institute of Neurology, University College London, 1 Wakefield Street, London, WC1N 1PJ, UK. r.guerreiro@ucl.ac.uk.
Genome Medicine
|October 21, 2015
Summary
Researchers found a gene variant (CCL11) linked to a 10-year delay in Alzheimer's disease onset. This discovery may lead to new treatments that could potentially halve the incidence of this common dementia.
Area of Science:
- Neuroscience
- Genetics
- Immunology
Background:
- Alzheimer's disease (AD) is the leading cause of dementia, characterized by cognitive decline.
- Advanced age is the primary risk factor for Alzheimer's disease.
- Genetic factors influencing the age of AD onset are of significant interest.
Purpose of the Study:
- To investigate genetic associations with the age of onset for Alzheimer's disease.
- To identify specific genetic variants potentially responsible for observed associations.
- To explore the functional role of identified variants in Alzheimer's disease pathogenesis.
Main Methods:
- Genome-wide association study (GWAS) to identify genetic loci associated with AD onset.
- Fine-mapping and sequencing to pinpoint specific variants within associated loci.
- Analysis of a protective haplotype and its association with delayed AD onset.
Main Results:
- A significant locus on chromosome 17 was associated with the age of Alzheimer's disease onset.
- A specific variant within the CCL11 gene is likely responsible for this association.
- A protective haplotype associated with a 10-year delay in AD onset was identified.
Conclusions:
- The CCL11 gene variant plays a potential role in modulating the age of Alzheimer's disease onset.
- Understanding the functional role of CCL11 may pave the way for novel therapeutic strategies.
- Development of immunomodulators targeting CCL11 could potentially reduce Alzheimer's disease incidence by 50%.
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