Decomposing socioeconomic inequality in poor mental health among Iranian adult population: results from the PERSIAN cohort study

Background Socioeconomic inequality in mental health in Iran is poorly understood. This study aimed to assess socioeconomic inequality in poor mental health among Iranian adults. Methods The study used the baseline data of PERSIAN cohort study including 131,813 participants from 17 geographically distinct areas of Iran. The Erreygers Concentration index (E) was used to quantify the socioeconomic inequalities in poor mental health. Moreover, we decomposed the E to identify factors contributing to the observed socioeconomic inequality in poor mental health in Iran. Results The estimated E for poor mental health was - 0.012 (95% CI: - 0.0144, - 0.0089), indicating slightly higher concentration of mental health problem among socioeconomically disadvantaged adults in Iran. Socioeconomic inequality in poor mental health was mainly explained by gender (19.93%) and age (12.70%). Region, SES itself, and physical activity were other important factors that contributed to the concentration of poor mental health among adults with low socioeconomic status. Conclusion There exists nearly equitable distribution in poor mental health among Iranian adults, but with important variations by gender, SES, and geography. These results suggested that interventional programs in Iran should focus on should focus more on socioeconomically disadvantaged people as a whole, with particular attention to the needs of women and those living in more socially disadvantaged regions. Keywords:Mental health; Socioeconomic inequality; Concentration index; Decompositio

A kinase-dead Csf1r mutation associated with adult-onset leukoencephalopathy has a dominant inhibitory impact on CSF1R signalling

Amino acid substitutions in the kinase domain of the human CSF1R gene are associated with autosomal dominant adult-onset leukoencephalopathy with axonal spheroids and pigmented glia (ALSP). To model the human disease, we created a disease-associated mutation (pGlu631Lys; E631K) in the mouse Csf1r locus. Homozygous mutation (Csf1rE631K/E631K) phenocopied the Csf1r knockout, with prenatal mortality or severe postnatal growth retardation and hydrocephalus. Heterozygous mutation delayed the postnatal expansion of tissue macrophage populations in most organs. Bone marrow cells from Csf1rE631K/+mice were resistant to CSF1 stimulation in vitro, and Csf1rE631K/+ mice were unresponsive to administration of a CSF1-Fc fusion protein, which expanded tissue macrophage populations in controls. In the brain, microglial cell numbers and dendritic arborisation were reduced in Csf1rE631K/+ mice, as in patients with ALSP. The microglial phenotype is the opposite of microgliosis observed in Csf1r+/- mice. However, we found no evidence of brain pathology or impacts on motor function in aged Csf1rE631K/+ mice. We conclude that heterozygous disease-associated CSF1R mutations compromise CSF1R signalling. We speculate that leukoencephalopathy associated with dominant human CSF1R mutations requires an environmental trigger and/or epistatic interaction with common neurodegenerative disease-associated alleles

Correction: Decomposing socioeconomic inequality in poor mental health among Iranian adult population: results from the PERSIAN cohort study

Following the publication of the original article [1], the authors would like to correct the code of the study in the ethics approval and consent to participate statement. The incorrect code of the study is: IR.KUMS.REC.1397.187 The correct code of the study is: IR.KUMS.REC.1397.866 The original articl