Parkinson's disease (PD) is a neurological disorder that affects dopaminergic neurons. The lack of understanding of the underlying molecular mechanisms of PD pathology makes treating it a challenge. Several pieces of evidence support the protective role of enriched environment (EE) and exercise on dopaminergic neurons. The specific aspect(s) of neuroprotection after exposure to EE have not been identified. Therefore, we have investigated the protective role of EE on dopamine dysregulation and subsequent downregulation of DJ1 protein using in vitro and in vivo models of PD. Our study for the first time demonstrated that DJ1 expression has a direct correlation with dopamine downregulation in PD models and exposure to EE has a significant impact on improving the behavioral changes in PD mice. This research provides evidence that exercise in EE has a positive effect on PD without interfering with the current line of therapy.

In addition to hemostasis and thrombosis, blood platelets are involved in various processes such as inflammation, infection, immunobiology, cancer metastasis, wound repair and angiogenesis. Platelets' hemostatic and non-hemostatic functions are mediated by the expression of various membrane receptors and the release of proteins, ions and other mediators. Therefore, specific activities of platelets responsible for the non-hemostatic disease are to be inhibited while leaving the platelet's hemostatic function unaffected. Platelets' anti-aggregatory property has been used as a primary criterion for antiplatelet drugs/bioactives; however, their non-hemostatic activities are not well known. This review describes the hemostatic and non-hemostatic function of human blood platelets and the modulatory effects of bioactive food components. PRACTICAL APPLICATIONS: In this review, we have discussed the antiplatelet effects of several food components. These bioactive compounds inhibit both hemostatic and non-hemostatic pathways involving blood platelet. Platelets have emerged as critical biological factors of normal and pathologic vascular healing and other diseases such as cancers and inflammatory and immune disorders. The challenge for therapeutic intervention in these disorders will be to find drugs and bioactive compounds that preferentially block specific sites implicated in emerging roles of platelets' complicated contribution to inflammation, tumour growth, or other disorders while leaving at least some of their hemostatic function intact.

Abstract The advent of cART has revolutionized the management of HIV-1 infection and saved the lives of millions of people worldwide. Yet, HIV-Associated Neurocognitive Disorder (HAND) continues to be clinically relevant with aging people with HIV-1 (PWH). The underlying mechanism of HAND remains poorly understood. In this regard Signal transducer and activator of transcription 1(STAT1) and interferon-induced protein with tetratricopeptide repeats 3 (IFIT3) genes have been shown to induce neuroinflammation and neuronal cell death. However, the role of IFIT3 in HAND pathology has not been well established. Therefore, the present work investigated the significant role of IFIT3 gene in the development of HAND. In the current study, we used an in-vitro model to expose the neuroblastoma cell-line SH-SY5Y with clinically relevant cARTs drug and HIV Tat protein to observe the STAT1 and IFIT3 genes dysregulation. Furthermore, study also investigates the STAT1 and IFIT3 protein dysregulation through immunocytochemistry and western blot assay. Overall observation indicated that HIV-Tat protein upregulated gene expression whereas with the cART exposure there was a downregulation of STAT1 and IFIT3 genes. We next aim to investigate the role of STAT1 and IFIT3 genes in HIV-induced neuroinflammation. The current study has established IFIT3 as a biomarker marker for the detection of HAND.