Dataset Information

Phishing vulnerability compounded by older age, apolipoprotein E e4 genotype, and lower cognition.

ABSTRACT: With technological advancements, financial exploitation tactics have expanded into the online realm. Older adults may be particularly susceptible to online scams due to age- and Alzheimer's disease-related changes in cognition. In this study, 182 adults ranging from 18 to 90 years underwent cognitive assessment, genotyping for apolipoprotein E e4 (APOE4), and completed the lab-based Short Phishing Email Suspicion Test (S-PEST) as well as the real-life PHishing Internet Task (PHIT). Across both paradigms, older age predicted heightened susceptibility to phishing, with this enhanced susceptibility pronounced among older APOE4 allele carriers with lower working memory. Additionally, performance in both phishing tasks was correlated in that reduced ability to discriminate between phishing and safe emails in S-PEST predicted greater phishing susceptibility in PHIT. The current study identifies older age, APOE4, and lower cognition as risk factors for phishing vulnerability and introduces S-PEST as an easy-to-administer, ecologically valid tool for assessing phishing susceptibility.

SUBMITTER: Pehlivanoglu D

PROVIDER: S-EPMC11309394 | biostudies-literature | 2024 Aug

REPOSITORIES: biostudies-literature

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Phishing vulnerability compounded by older age, apolipoprotein E e4 genotype, and lower cognition.

Pehlivanoglu Didem D Shoenfelt Alayna A Hakim Ziad Z Heemskerk Amber A Zhen Jialong J Mosqueda Mario M Wilson Robert C RC Huentelman Matthew M Grilli Matthew D MD Turner Gary G Spreng R Nathan RN Ebner Natalie C NC

PNAS nexus 20240801 8

With technological advancements, financial exploitation tactics have expanded into the online realm. Older adults may be particularly susceptible to online scams due to age- and Alzheimer's disease-related changes in cognition. In this study, 182 adults ranging from 18 to 90 years underwent cognitive assessment, genotyping for apolipoprotein E e4 (APOE4), and completed the lab-based Short Phishing Email Suspicion Test (S-PEST) as well as the real-life PHishing Internet Task (PHIT). Across both p ...[more]

PMID: 39118834

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Project description:In addition to being the greatest genetic risk factor for Alzheimer's disease, expression of the ɛ4 allele of apolipoprotein E can lead to cognitive decline during ageing that is independent of Alzheimer's amyloid-β and tau pathology. In human post-mortem tissue and mouse models humanized for apolipoprotein E, we examined the impact of apolipoprotein E4 expression on brain exosomes, vesicles that are produced within and secreted from late-endocytic multivesicular bodies. Compared to humans or mice homozygous for the risk-neutral ɛ3 allele we show that the ɛ4 allele, whether homozygous or heterozygous with an ɛ3 allele, drives lower exosome levels in the brain extracellular space. In mice, we show that the apolipoprotein E4-driven change in brain exosome levels is age-dependent: while not present at age 6 months, it is detectable at 12 months of age. Expression levels of the exosome pathway regulators tumor susceptibility gene 101 (TSG101) and Ras-related protein Rab35 (RAB35) were found to be reduced in the brain at the protein and mRNA levels, arguing that apolipoprotein E4 genotype leads to a downregulation of exosome biosynthesis and release. Compromised exosome production is likely to have adverse effects, including diminishing a cell's ability to eliminate materials from the endosomal-lysosomal system. This reduction in brain exosome levels in 12-month-old apolipoprotein E4 mice occurs earlier than our previously reported brain endosomal pathway changes, arguing that an apolipoprotein E4-driven failure in exosome production plays a primary role in endosomal and lysosomal deficits that occur in apolipoprotein E4 mouse and human brains. Disruption of these interdependent endosomal-exosomal-lysosomal systems in apolipoprotein E4-expressing individuals may contribute to amyloidogenic amyloid-β precursor protein processing, compromise trophic signalling and synaptic function, and interfere with a neuron's ability to degrade material, all of which are events that lead to neuronal vulnerability and higher risk of Alzheimer's disease development. Together, these data suggest that exosome pathway dysfunction is a previously unappreciated component of the brain pathologies that occur as a result of apolipoprotein E4 expression.

Dataset Information

Phishing vulnerability compounded by older age, apolipoprotein E e4 genotype, and lower cognition.

Publications

Phishing vulnerability compounded by older age, apolipoprotein E e4 genotype, and lower cognition.

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