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Exploring the Role of HSV-1 in the Pathogenesis of Alzheimer’s Disease
No full textAlzheimer’s Disease (AD) is the most common neurodegenerative disorder, characterized by excessive amyloid beta(Aβ) plaque and tau protein tangles in the brain. While the exact cause of AD remains unclear, recent research implicates viral vectors, particularly Herpes Simplex Virus 1 (HSV-1), in its progression. This review investigates how HSV-1 infection can contribute to the development and transmission of AD through viral mechanisms, including pathological amyloid beta and tau protein deposition. A systematic review of 30 peer reviewed articles from the past 10 years was conducted, focusing on HSV-1’s influence in AD, using databases such as PubMed and Google Scholar with keywords ‘HSV-1,’ ‘AD,’ ‘amyloid beta,’ and ‘tau protein.’ Findings indicate HSV-1 contributes to AD pathology, evidenced by HSV-1 DNA in AD patients’ brain. A meta-analysis revealed HSV-1 infection is associated with an increased risk of AD, with a pooled odds ratio (OR) of 1.40. These observations suggest HSV-1 promotes Aβ and hyperphosphorylated tau protein accumulation via viral effects like neuroinflammation. This review supports the hypothesis that HSV-1 plays a significant role in AD development, offering new insights into disease progression. Targeting HSV-1 and its pathways may offer novel therapeutic strategies for preventing AD. Further research is needed to examine HSV-1’s long-term effects on neurons and develop interventions that mitigate its impact on AD. Understanding the role of HSV-1 in transmitting AD could pave the way for future research investigating novel therapeutic and preventive strategies that target the viral interactions that lead to Alzheimer’s pathology
Impact of STAT3 Inhibition on Tumour Progression and Immune Evasion in Non-Small Cell Lung Cancer
No full textSignal Transducer and Activator of Transcription 3 (STAT3) is a critical transcription factor that regulates cell growth, survival and immune responses. It is implicated in Non-Small Cell Lung Cancer (NSCLC), the most prevalent form of lung cancer categorized by aggressive tumour progression and high metastatic potential. NSCLC’s aggressiveness stems from the overactivation of STAT3, promoting cancer cell proliferation, survival, and invasion through mechanisms including genetic mutations, cytokine signalling and inflammatory pathways within the tumour microenvironment. This heightened STAT3 activity not only supports tumour growth but also suppresses anti-tumour immune responses and fosters an immunosuppressive environment. Currently, treatment for NSCLC patients involves cancer therapies that reduce tumour cell proliferation. This study investigates the impact of STAT3 inhibition in NSCLC that suppresses the anti-tumour immunity and epithelial-mesenchymal transition in the cancer cells. This article utilizes the PubMed database to retrieve a total of twenty articles regarding the effects of STAT3 on cell growth and metastasis, specific STAT3 inhibitors such as W2014-S, IL-37, MicroRNA-148a, RITA and WP1066, and investigating their effects on NSCLC. Inhibiting STAT3 reduces tumour cell proliferation while enhancing T-cell activation and reducing immunosuppressive factors within the tumour microenvironment. Some studies observed the role of STAT3 inhibitors with both in vitro and in vivo samples, highlighting the therapeutic potential. STAT3 clearly has a crucial role in aggressive pathogenesis seen in NSCLC due to increased immune evasion; thus, the inhibition would help reduce the tumour invasiveness, offering a promising therapeutic approach to mitigate NSCLC progression and enhancing the efficacy of existing treatments
HCSO Child Protective Investigator Badge
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HCSO Sheriff Explorer Badge - Gold
No full texthttps://digitalcommons.usf.edu/idex_hcso/1061/thumbnail.jp
