Neutrophil populations were plotted in histogram form, and the average fluorescence intensity from each sample was plotted as the percentage of the antigen expression. MicroRNAs fine-tune gene expression at the posttranscriptional level thereby regulating various cellular processes. They bind to the 39 untranslated region of target mRNAs and recruit the RNA-induced silencing complex to downregulate expression of the target. MiRs have emerged as important regulators of neuronal function, their altered expression contributing to neuronal dysfunction in diseases of the central nervous system, including HIV-associated neurocognitive disorders. Since HIV does not infect neurons, the neuronal pathology of HAND is secondary to CNS inflammation. In recent years, implementation of combined antiretroviral therapy has resulted in lower plasma and CSF viral load and higher CD4+ cell counts in HIV infected patients. Therefore, HIV-infected patients now live longer. However, this chronicity may further pre-dispose them to agerelated cognitive impairment and the prevalence of HAND has increased despite implementation of cART. One pathological manifestation of HIV infection that can lead to a severe form of HAND is HIV encephalitis, where inflammatory AbMole Folic acid cytokines and chemokines as well as HIV proteins cause changes in neuronal gene expression, leading to neuronal dysfunction and death. Elucidation of novel molecular mechanisms that contribute to the neuronal dysfunction in HIVE is necessary, as it will provide insights into pathogenesis of not only HAND, but also other degenerative diseases associated with CNS inflammation. Alteration of the brain miR expression profile in HIVE and its non-human primate model has been reported in previous studies. Among the miRs that were found to be AbMole Nitroprusside disodium dihydrate differentially expressed in the disease condition compared to uninfected control samples, miR-142 was upregulated both in the frontal cortex white matter in humans, as well as in the caudate nucleus and hippocampus in monkeys and caudate nucleus in humans. In a previous study we showed that in the brain, miR-142 is upregulated within neurons and macrophage/microglia nodules in SIVE. We also identified the NAD-dependent deacetylase Sirtuin1 as a direct target for miR-142-5p, one of the two functional mature forms of miR-142. MiR-142 has been extensively studied in the hematopoietic cell lineage, where it regulates differentiation of T lymphocytes and myeloid cells. In addition to SIVE, miR142 expression in neurons has been reported following nerve crush injury and cocaine treatment. However, very little is known about downstream effects of chronic miR-142 upregulation in neuronal cells.Blinding of the clinical biopsy samples for pathological.