Summary There is a long way to go before the coronavirus disease 2019 (Covid‐19) outbreak comes under control. qRT‐PCR is currently used for the detection of severe acute respiratory syndrome coronavirus 2 (SARS‐CoV‐2), the causative agent of Covid‐19, but it is expensive, time‐consuming, and not as sensitive as it should be. Finding a rapid, easy‐to‐use, and cheap diagnostic method is necessary to help control the current outbreak. Microfluidic systems provide a platform for many diagnostic tests, including RT‐PCR, RT‐LAMP, nested‐PCR, nucleic acid hybridization, ELISA, fluorescence‐Based Assays, rolling circle amplification, aptamers, sample preparation multiplexer (SPM), Porous Silicon Nanowire Forest, silica sol‐gel coating/bonding, and CRISPR. They promise faster, cheaper, and easy‐to‐use methods with higher sensitivity, so microfluidic devices have a high potential to be an alternative method for the detection of viral RNA. These devices have previously been used to detect RNA viruses such as H1N1, Zika, HAV, HIV, and norovirus, with acceptable results. This paper provides an overview of microfluidic systems as diagnostic methods for RNA viruses with a focus on SARS‐CoV‐2.
Background Parkinson’s disease (PD) is the second most prevalent neurodegenerative disorder, characterized by motor and non-motor symptoms, significantly affecting patients’ life. Pathologically, PD is associated with the extensive degeneration of dopaminergic neurons in various regions of the central nervous system (CNS), specifically the substantia nigra. This neuronal loss is accompanied by the aggregation of misfolded protein, named α-synuclein. Main text Recent studies detected several clues of neuroinflammation in PD samples using postmortem human PD brains and various PD animal models. Some evidence of neuroinflammation in PD patients included higher levels of proinflammatory cytokines in serum and cerebrospinal fluid (CSF), presence of activated microglia in various brain regions such as substantia nigra, infiltration of peripheral inflammatory cells in affected brain regions, and altered function of cellular immunity like monocytes phagocytosis defects. On the other side, Toll-like receptors (TLRs) are innate immune receptors primarily located on microglia, as well as other immune and non-immune cells, expressing pivotal roles in recognizing exogenous and endogenous stimuli and triggering inflammatory responses. Most studies indicated an increased expression of TLRs in the brain and peripheral blood cells of PD samples. Besides, this upregulation was associated with excessive neuroinflammation followed by neurodegeneration in affected regions. Therefore, evidence proposed that TLR-mediated neuroinflammation might lead to a dopaminergic neural loss in PD patients. In this regard, TLR2, TLR4, and TLR9 have the most prominent roles. Conclusion Although the presence of inflammation in acute phases of PD might have protective effects concerning the clearance of α-synuclein and delaying the disease advancement, the chronic activation of TLRs and neuroinflammation might lead to neurodegeneration, resulting in the disease progression. Therefore, this study aimed to review additional evidence of the contribution of TLRs and neuroinflammation to PD pathogenesis, with the hope that TLRs could serve as novel disease-modifying therapeutic targets in PD patients in the future.
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