This study aims to provide clinical and scientific information about the effects of various anti-inflammatory medicines on patients with cardiovascular disease (CVD). We also discussed the anti-inflammatory strategies and molecular mechanisms being investigated in preclinical or clinical CVD research. Numerous studies on anti-inflammatory medicines for CVD have resulted from greater knowledge of how innate and adaptive immunity influence plaque development and rupture. Some of these are now being evaluated in clinical trials and use lower dosages of existing medications that were initially developed for other inflammatory disorders with a high risk of CVD such as rheumatoid arthritis and psoriasis. Other research includes retrospective and meta-analyses of clinical trials that examine the risk of CVD among individuals with various inflammatory diseases. We also included natural bioactive compounds nanodrug and multiomics approaches to treat CVD by utilizing inflammatory pathways. Chronic subclinical inflammation is a major contributor to the development of CVD and has been associated with both the onset and progression of atherosclerosis. Several pro-inflammatory cytokines including C-reactive protein (CRP) tumor necrosis factor-alpha (TNF-α) interleukins-1 and 6 (IL-1 and IL-6) leukotrienes and adiponectin have been identified as independent risk factors for coronary heart disease and promoters of arterial development. Researchers are looking for ways to stop the different inflammatory pathways that lead to atherosclerosis. These include multiomics approach antioxidants phospholipase A2 inhibitors leukotriene pathway inhibitors Phospholipase A2 (PLA2) inhibitors non-inhibitors anti-inflammatory drugs (like methotrexate) IL-1 inhibitors and p-selectin inhibitors.

Parkinson's disease (PD) is a neurodegenerative disorder characterized by motor symptoms such as tremors stiffness and bradykinesia as well as non-motor symptoms like cognitive impairment and mood swings. PD is a multifactorial disease comprised of environmental and genetic etiologies. In addition to family history Variants in the LRRK2 gene are important as they represent the most common cause of familial PD and are also associated with some sporadic cases. The underlying causes of PD are also numerous and can be divided into a variety of environmental and genetic factors. This is the most relevant part because the LRRK2 gene Variant is one of the most common causes of familial Parkinson's disease as well as contributing to sporadic cases beyond hereditary factors. Pathogenic LRRK2 variants result in the dysfunction of LRRK2 disrupting cellular pathways and potentially driving neurodegeneration. The purpose of the current study was to examine in depth the complex network of LRRK2-regulated signalling pathways and how they collectively modulate changes in neuronal survival and function. These LRRK2 variants are causing cell homeostasis disturbances due to dysfunction of interaction between key proteins such as α-synuclein and tau that have been implicated in Parkinson's development. In addition we will explore what other therapies could be targeted to mitigate the role of LRRK2-mediated processes in PD such as kinase inhibitors and other process-targeted treatments.

About 70% of dementia cases are caused by Alzheimer's disease (AD) making it the most common cause. Nearly 7 million people in the US currently have AD and by 2050 that number is expected to nearly double creating serious socioeconomic problems. A cure for AD is still elusive despite a great deal of research. Numerous signaling pathways linked to AD neuropathology have been the subject of recent studies with glycogen synthase kinase-3β (GSK3-β) emerging as a potential therapeutic target. GSK3-β is a constitutively active serine/threonine kinase that is essential for many biological functions such as gene transcription and glycogen metabolism. It has a complex role in the pathophysiology of AD impacting important indicators like tau phosphorylation amyloid-β production neuroinflammation memory loss and synaptic dysfunction. The goal of this review article is to give a thorough overview of GSK3-β neurobiology with a focus on how it affects signaling pathways linked to the pathophysiology of AD. It also evaluates the feasibility of targeting GSK3-β as a therapeutic approach for AD by examining the state of GSK3-β inhibitor development in preclinical and clinical trials. Preclinical research has shown encouraging results but there are still obstacles in converting these discoveries into successful clinical therapies including problems with drug specificity safety and brain penetration. However there is still hope for creating new therapeutic strategies to fight this debilitating neurodegenerative disease thanks to continued research into GSK3-β inhibitors.