Abstract
BackgroundNeuroticism is a core personality trait and a major risk factor for several mental and physical diseases, particularly in females, who score higher on neuroticism than men, on average. However, a better understanding of the expression profiles of proteins in the circulating blood of different neurotic female populations may help elucidate the intrinsic mechanism of neurotic personality and aid prevention strategies on mental and physical diseases associated with neuroticism.MethodsIn our study, female subjects were screened for inclusion by the Eysenck Personality Questionnaire (EPQ), Beck Depression Inventory (BDI), Beck Anxiety Inventory (BAI) scales and routine physical examination. Subjects who passed the examination and volunteered to participate were grouped by neuroticism using EPQ scores (0 and 1 = low neuroticism group; > 5 = high neuroticism group). Proteins in serum samples of the two neuroticism groups were identified using isobaric tags for relative and absolute quantification (iTRAQ) technology.ResultsA total of 410 proteins exhibited significant differences between high and low neuroticism, 236 proteins were significantly upregulated and 174 proteins were significantly downregulated. Combine the results of GO and KEGG enrichment analysis of differences proteins between high and low neuroticism with the PPI network, it could be observed that the Alpha-synuclein (SNCA), ATP7A protein (ATP7A), Guanine nucleotide-binding protein G(I)/G(S)/G(O) subunit gamma-2 (GNG2), cyclin-dependent kinase 6 (CDK6), myeloperoxidase (MPO), azurocidin (AZU1), Histone H2B type 1-H (HIST1H2BH), Integrin alpha-M (ITGAM) and Matrix metalloproteinase-9 (MMP9) might participate in the intrinsic mechanism of neuroticism by regulating response to catecholamine stimulus, catecholamine metabolic process, limbic system development and transcriptional misregulation in cancer pathway.ConclusionsOur study revealed the characteristics of the neurotic personality proteome, which might be intrinsic mechanism of the neurotic population.
Highlights
Neuroticism is a core personality trait and a major risk factor for several mental and physical diseases, in females, who score higher on neuroticism than men, on average
From the results of bioinformatics analysis of differences in proteins between high and low neuroticism, we found that SNCA, ATP7A, G(O) subunit gamma-2 (GNG2), cyclin-dependent kinase 6 (CDK6), MPO, AZU1, HIST1H2BH, Integrin alpha-M (ITGAM) and Matrix metalloproteinase-9 (MMP9) might participate in the intrinsic mechanism of neuroticism by regulating response to catecholamine stimulus, catecholamine metabolic process, limbic system development and transcriptional misregulation in cancer pathway
We found that GNG2, ATP7A and SNCA were significantly upregulated in high vs. low neuroticism and enriched in the pathways related to response to catecholamine stimulus
Summary
Neuroticism is a core personality trait and a major risk factor for several mental and physical diseases, in females, who score higher on neuroticism than men, on average. Neuroticism is a core personality dimension and is operationally defined as the tendency to experience negative emotions [1]. This trait is considered a measure of emotional instability. High neuroticism is an independent risk factor for cardiovascular disease, and closely associated with the morbidity and mortality of chronic diseases such as cancer and diabetes [10, 11]. One prospective study on individuals with chronic renal insufficiency found that patients with high levels of neuroticism had an estimated upper mortality rate of 37.5% [12]. Women score higher on neuroticism than men, on average, and have a higher incidence of major emotional disorders
Sign-in/Register to view highlights & summary Sign-in/Register to access full text options 
Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
