Although recent research has begun to describe the neural and genetic processes underlying variability in responses to trauma, less is known about how these processes interact. We addressed this issue by using functional magnetic resonance imaging to examine the relationship between posttraumatic stress symptomatology (PTSS), a common genetic polymorphism of the serotonin transporter [5-HTT (5-hydroxy tryptamine)] gene and neural activity in response to viewing images associated with the 9/11 terrorist attack among a rare sample of high-exposure 9/11 survivors (n = 17). Participants varied in whether they carried a copy of the short allele in the promoter region of the 5-HTT gene. During scanning, participants viewed images of the 9/11 attack, non-9/11 negative and neutral images. Three key findings are reported. First, carriers of the short allele displayed higher levels of PTSS. Second, both PTSS and the presence of the short allele correlated negatively with activity in a network of cortical midline regions (e.g. the retrosplenal and more posterior cingulate cortices (PCCs)) implicated in episodic memories and self-reflection when viewing 9/11 vs non-9/11 negative control images. Finally, exploratory analyses indicated that PCC activity mediated the relationship between genotype and PTSS. These results highlight the role of PCC in distress following trauma.
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http://dx.doi.org/10.1093/scan/nsu125 | DOI Listing |
Forensic Sci Int Genet
January 2025
Forensic DNA Division, National Forensic Service, Wonju, South Korea. Electronic address:
Y-chromosomal short tandem repeats (Y-STRs) at rapidly mutating (RM) loci have been suggested as tools for differentiating paternally related males. RMplex is a recently developed system that incorporates 26 RM loci and four fast-mutating (FM) loci, targeting 44 male-specific loci. Here, we evaluated the RMplex by estimating Y-STR mutation rates and the overall differentiation rates for 542 Korean father-son pairs, as well as the genetic population values for 409 unrelated males.
View Article and Find Full Text PDFBackground: Apolipoprotein ε4 allele (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) with females having higher risk than males. Compared with non-carriers, cognitively normal, middle-aged APOE4 carriers have lower cerebral blood flow (CBF) decades before clinical symptoms appear. Early intervention to protect CBF would be critical for APOE4 carriers to mitigate AD progression.
View Article and Find Full Text PDFBackground: Apolipoprotein ε4 allele (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD). Compared with non-carriers, cognitively normal APOE4 individuals have shown brain atrophy and lower cerebral blood flow (CBF) decades before AD pathological and clinical symptoms appear. The goal of the study is to determine if using Sirolimus, an FDA-approved mTOR inhibitor, could restore the brain volumes in structures related to cognitive functions and global CBF (gCBF) for asymptomatic APOE4 carriers compared with non-carriers.
View Article and Find Full Text PDFBackground: Alzheimer's disease (AD) is a neurodegenerative disease characterized by progressive cognitive decline. APOE-ε4 has been identified as the most prevalent genetic risk factor for the early onset of AD, while ABCA7-80 (rs115550680) has been shown to have a stronger effect size than the APOE-ε4 allele and is associated with the development of late-onset of AD among African Americans. Although the efficiency of executive functions declines with age, some basic attentional functions and preserved knowledge may help mitigate the effects of aging on working memory.
View Article and Find Full Text PDFAlzheimers Dement
December 2024
University of Missouri, Columbia, MO, USA.
Background: Apolipoprotein e4 allele (APOE4) is the strongest genetic risk factor for late-onset Alzheimer's disease (AD) with females having higher risk than males. Compared with non-carriers, cognitively normal, middle-aged APOE4 carriers have lower cerebral blood flow (CBF) decades before clinical symptoms appear. Early intervention to protect CBF would be critical for APOE4 carriers to mitigate AD progression.
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