Genetic Association between Alzheimer’s Disease Risk Variant of the PICALM Gene and Auditory Event-Related Potentials in Aging
- Authors: Ponomareva N.V.1,2, Andreeva T.V.2,3, Protasova M.A.2, Filippova Y.V.1, Kolesnikova E.P.1, Fokin V.F.1, Illarioshkin S.N.1, Rogaev E.I.2,3,4
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Affiliations:
- Research Center for Neurology
- Vavilov Institute of General Genetics
- Department of Biology, Center of Genetics and Genetic Technologies
- Brudnick Neuropsychiatric Research Institute, Department of Psychiatry
- Issue: Vol 83, No 9 (2018)
- Pages: 1075-1082
- Section: Article
- URL: https://journals.rcsi.science/0006-2979/article/view/151716
- DOI: https://doi.org/10.1134/S0006297918090092
- ID: 151716
Cite item
Abstract
Aging and genetic predisposition are major risk factors in age-related neurodegenerative disorders. The most common neurodegenerative disorder is Alzheimer’s disease (AD). Genome-wide association studies (GWAS) have identified statistically significant association of the PICALM rs3851179 polymorphism with AD. The PICALM G allele increases the risk of AD, while the A allele has a protective effect. We examined the association of the PICALM rs3851179 polymorphism with parameters of the P3 component of auditory event-related potentials (ERPs) in 87 non-demented volunteers (age, 19–77 years) subdivided into two cohorts younger and older than 50 years of age. We found statistically significant association between the AD risk variant PICALM GG and increase in the P3 latency in subjects over 50 years old. The age-dependent increase in the P3 latency was more pronounced in the PICALM GG carriers than in the carriers of the PICALM AA and PICALM AG genotypes. The observed PICALM-associated changes in the neurophysiological processes indicate a decline in the information processing speed with aging due, probably, to neuronal dysfunction and subclinical neurodegeneration of the neuronal networks in the hippocampus and the frontal and parietal cortical areas. Such changes were less pronounced in the carriers of the PICALM gene A allele, which might explain the protective effect of this allele in the cognitive decline and AD development.
About the authors
N. V. Ponomareva
Research Center for Neurology; Vavilov Institute of General Genetics
Author for correspondence.
Email: ponomareva@neurology.ru
Russian Federation, Moscow, 125367; Moscow, 119991
T. V. Andreeva
Vavilov Institute of General Genetics; Department of Biology, Center of Genetics and Genetic Technologies
Email: rogaev@vigg.ru
Russian Federation, Moscow, 119991; Moscow, 119991
M. A. Protasova
Vavilov Institute of General Genetics
Email: rogaev@vigg.ru
Russian Federation, Moscow, 119991
Yu. V. Filippova
Research Center for Neurology
Email: rogaev@vigg.ru
Russian Federation, Moscow, 125367
E. P. Kolesnikova
Research Center for Neurology
Email: rogaev@vigg.ru
Russian Federation, Moscow, 125367
V. F. Fokin
Research Center for Neurology
Email: rogaev@vigg.ru
Russian Federation, Moscow, 125367
S. N. Illarioshkin
Research Center for Neurology
Email: rogaev@vigg.ru
Russian Federation, Moscow, 125367
E. I. Rogaev
Vavilov Institute of General Genetics; Department of Biology, Center of Genetics and Genetic Technologies; Brudnick Neuropsychiatric Research Institute, Department of Psychiatry
Author for correspondence.
Email: rogaev@vigg.ru
Russian Federation, Moscow, 119991; Moscow, 119991; Worcester