Polymorphism in the genomic region harboring the CLU gene (rs11136000) has been associated with the risk for Alzheimer's disease (AD). CLU C allele is assumed to confer risk for AD and the allele T may have a protective effect. We investigated the influence of the AD-associated CLU genotype on a common neurophysiological trait of brain activity (resting-state alpha-rhythm activity) in non-demented adults and elucidated whether this influence is modified over the course of aging. We examined quantitative electroencephalography (EEG) in a cohort of non-demented individuals (age range 20-80) divided into young (age range 20-50) and old (age range 51-80) cohorts and stratified by CLU polymorphism. To rule out the effect of the apolipoprotein E (ApoE) genotype on EEG characteristics, only subjects without the ApoE ε4 allele were included in the study. The homozygous presence of the AD risk variant CLU CC in non-demented subjects was associated with an increase of alpha3 absolute power. Moreover, the influence of CLU genotype on alpha3 was found to be higher in the subjects older than 50 years of age. The study also showed age-dependent alterations of alpha topographic distribution that occur independently of the CLU genotype. The increase of upper alpha power has been associated with hippocampal atrophy in patients with mild cognitive impairment (Moretti etal., 2012a). In our study, the CLU CC-dependent increase in upper alpha rhythm, particularly enhanced in elderly non-demented individuals, may imply that the genotype is related to preclinical dysregulation of hippocampal neurophysiology in aging and that this factor may contribute to the pathogenesis of AD.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC3861782 | PMC |
http://dx.doi.org/10.3389/fnagi.2013.00086 | DOI Listing |
Hematology
December 2025
Department of Pediatrics, The First Affiliated Hospital of Guangxi Medical University, Nanning, People's Republic of China.
Objectives: This study aims to investigate the serotransferrin (TF), complement C1s subcomponent (C1S), immunoglobulin heavy constant gamma 4 (IGHG4), hemoglobin subunit alpha (HBA1), and clusterin (CLU) contents in β-thalassemia patients, and explores their physiological role as potential non-invasive bioindicators for disease diagnosis and iron overload.
Methods: A total of 62 children with β-thalassemia were recruited and categorized by genotype, along with 17 healthy pediatric volunteers for analysis. The circulating ferritin content was evaluated, and plasma levels of TF, C1S, IGHG4, HBA1, and CLU were assessed using ELISA.
Int J Mol Sci
November 2024
Department of Bionano Technology, Gachon Medical Research Institute, Gachon University, Seongnam 13120, Republic of Korea.
Alzheimer's disease (AD) is a complex neurodegenerative disorder influenced by various genetic factors. In addition to the well-established amyloid precursor protein (), Presenilin-1 (), Presenilin-2 (), and apolipoprotein E (), several other genes such as Sortilin-related receptor 1 (), Phospholipid-transporting ATPase ABCA7 (), Triggering Receptor Expressed on Myeloid Cells 2 (), Phosphatidylinositol-binding clathrin assembly protein (), and clusterin () were implicated. These genes contribute to neurodegeneration through both gain-of-function and loss-of-function mechanisms.
View Article and Find Full Text PDFJ Nephrol
December 2024
Institute of Molecular Biology and Genetics (Biogem), Ariano Irpino, Italy.
This review discusses genetic variants associated with cognitive dysfunction in chronic kidney disease (CKD) patients, emphasising the limited research in this area. Four studies have explored genetic markers of cognitive dysfunction in CKD, with findings suggesting shared genetic biomarkers between Alzheimer's Disease and CKD.Because of the limited specific research on genetic markers of cognitive dysfunction and dementia in CKD, we extracted data from the current literature studies on genetic markers in the general population that may be relevant to the CKD population.
View Article and Find Full Text PDFPeerJ
May 2024
School of Allied Health Sciences, College of Graduate Studies, Walailak University, Nakhon Si Thammarat, Thailand.
Background: Alzheimer's disease (AD) is one of the multifaceted neurodegenerative diseases influenced by many genetic and epigenetic factors. Genetic factors are merely not responsible for developing AD in the whole population. The studies of genetic variants can provide significant insights into the molecular basis of Alzheimer's disease.
View Article and Find Full Text PDFGenes (Basel)
August 2023
Biodemography of Aging Research Unit, Social Science Research Institute, Duke University, Durham, NC 27705, USA.
Sporadic Alzheimer's disease (AD) is a polygenic neurodegenerative disorder. Single-nucleotide polymorphisms (SNPs) in multiple genes (e.g.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!