Pyroptosis in lung cancer: The emerging role of non-coding RNAs.

Lung cancer remains an intractable malignancy worldwide, prompting novel therapeutic modalities. Pyroptosis, a lethal form of programmed cell death featured by inflammation, has been involved in cancer progression and treatment response. Simultaneously, non-coding RNA has been shown to have important roles in coordinating pattern formation and oncogenic pathways, including long non-coding RNA (lncRNAs), microRNA (miRNAs), circular RNA (circRNAs), and small interfering RNA (siRNAs). Recent studies have revealed that ncRNAs can promote or inhibit pyroptosis by interacting with key molecular players such as NLRP3, GSDMD, and various transcription factors. This dual role of ncRNAs offers a unique therapeutic potential to manipulate pyroptosis pathways, providing opportunities for innovative cancer treatments. In this review, we integrate current research findings to propose novel strategies for leveraging ncRNA-mediated pyroptosis as a therapeutic intervention in lung cancer. We explore the potential of ncRNAs as biomarkers for predicting patient response to treatment and as targets for overcoming resistance to conventional therapies.

Deciphering NF-kappaB pathways in smoking-related lung carcinogenesis.

One of the main causes of death worldwide is lung cancer, which is largely caused by cigarette smoking. The crucial transcription factor NF-κB, which controls inflammatory responses and various cellular processes, is a constitutively present cytoplasmic protein strictly regulated by inhibitors like IκB proteins. Upon activation by external stimuli, it undergoes phosphorylation, translocates into the nucleus, and modulates the expression of specific genes. The incontrovertible association between pulmonary malignancy and tobacco consumption underscores and highlights a public health concern. Polycyclic aromatic hydrocarbons and nitrosamines, potent carcinogenic compounds present in the aerosol emitted from combusted tobacco, elicit profound deleterious effects upon inhalation, resulting in severe perturbation of pulmonary tissue integrity. The pathogenesis of smoking-induced lung cancer encompasses an intricate process wherein NF-κB activation plays a pivotal role, triggered by exposure to cigarette smoke through diverse signaling pathways, including those associated with oxidative stress and pro-inflammatory cytokines. Unraveling the participation of NF-κB in smoking-induced lung cancer provides pivotal insights into molecular processes, wherein intricate crosstalk between NF-κB and pathways such as MAPK and PI3K-Akt amplifies the inflammatory response, fostering an environment conducive to the formation of lung cancer. This study reviews the critical function of NF-κB in the complex molecular pathways linked to the initiation and advancement of lung carcinogenesis as well as potential treatment targets. See also the graphical abstract(Fig. 1).

Delineating the NOX-Mediated Promising Therapeutic Strategies for the Management of Various Cardiovascular Disorders: A Comprehensive Review.

Cardiovascular disorders (CVDs) are reported to occur with very high rates of incidence and exhibit high morbidity and mortality rates across the globe. Therefore, research is focused on searching for novel therapeutic targets involving multiple pathophysiological mechanisms. Oxidative stress plays a critical role in the development and progression of various CVDs, such as hypertension, pulmonary hypertension, heart failure, arrhythmia, atherosclerosis, ischemia-reperfusion injury, and myocardial infarction. Among multiple pathways generating reactive oxygen species (ROS), NADPH defines all abbreviations oxidases of the NOX family as the major source of ROS generation and plays an intricate role in the development and progression of CVDs. Therefore, exploring the role of different NADPH oxidase isoforms in various cardiovascular pathologies has attracted attention to current cardiovascular research. Focusing on NADPH oxidases to reduce oxidative stress in managing diverse CVDs may offer unique therapeutic approaches to prevent and treat various heart conditions. The current review article highlights the role of different NADPH oxidase isoforms in the pathophysiology of various CVDs. Moreover, the focus is also to emphasize different experimental studies that utilized various NADPH oxidase isoform modulators to manage other disorders. The present review article considers new avenues for researchers/scientists working in the field of cardiovascular pharmacology utilizing NADPH oxidase isoform modulators.

Nrf2 pathways in neuroprotection: Alleviating mitochondrial dysfunction and cognitive impairment in aging.

Mitochondrial dysfunction and cognitive impairment are widespread phenomena among the elderly, being crucial factors that contribute to neurodegenerative diseases. Nuclear factor erythroid 2-related factor 2 (Nrf2) is an important regulator of cellular defense systems, including that against oxidative stress. As such, increased Nrf2 activity may serve as a strategy to avert mitochondrial dysfunction and cognitive decline. Scientific data on Nrf2-mediated neuroprotection was collected from PubMed, Google Scholar, and Science Direct, specifically addressing mitochondrial dysfunction and cognitive impairment in older people. Search terms included "Nrf2", "mitochondrial dysfunction," "cognitive impairment," and "neuroprotection." Studies focusing on in vitro and in vivo models and clinical investigations were included to review Nrf2's therapeutic potential comprehensively. The relative studies have demonstrated that increased Nrf2 activity could improve mitochondrial performance, decrease oxidative pressure, and mitigate cognitive impairment. To a large extent, this is achieved through the modulation of critical cellular signalling pathways such as the Keap1/Nrf2 pathway, mitochondrial biogenesis, and neuroinflammatory responses. The present review summarizes the recent progress in comprehending the molecular mechanisms regarding the neuroprotective benefits mediated by Nrf2 through its substantial role against mitochondrial dysfunction and cognitive impairment. This review also emphasizes Nrf2-target pathways and their contribution to cognitive function improvement and rescue from mitochondria-related abnormalities as treatment strategies for neurodegenerative diseases that often affect elderly individuals.

Nerolidol- Potential Therapeutic Agent for Various Neurological Disorders via its Antioxidative Property.

Neurological disorders are devastating conditions affecting both cognitive and motorrelated functions in aged people. Yet there is no proper medication to treat these illnesses, and the currently available medications can only provide symptomatic relief to the patients. All neurological disorders share the same etiology, such as oxidative stress, mitochondrial dysfunction, neurochemical deficiency, neuronal loss, apoptosis, endoplasmic reticulum stress, neuroinflammation, and disease-related protein aggregation. Nowadays, researchers use antioxidant-based strategies to prevent or halt the disease progression. Nerolidol, a strong antioxidant, possesses various biological activities and properties that treat cardiotoxicity, nephrotoxicity, neurotoxicity, and many other diseases. Many recent publications and research studies highlight the beneficial effect of nerolidol on brain disorders. In Alzheimer's disease, nerolidol shows neuroprotection by decreasing amyloid plaque formation, lipid peroxidation, cholinergic neuronal loss, locomotor dysfunction, neuroinflammation, and hippocampal damage via enhancing antioxidant expression. Also, it shows neuroprotection against rotenone-induced neurotoxicity by inhibiting microglial activation. Another study reported that nerolidol shows antiepileptic effects in animal models by suppressing kindling-induced memory impairment by decreasing oxidative stress. It has been found that NRL administration increases the antioxidant levels, decreasing the proinflammatory cytokine release as well as decreasing the apoptotic protein and cerebral infarct size. In conclusion, nerolidol tends to reverse the harmful effects of disease-related factors, including OS, neuroinflammation, protein aggregation, and apoptosis, making nerolidol a choiceable drug for the management of neurological disorders. The purpose of this review is to discuss the mechanism of nerolidol in treating various neurological disorders.

Plumbagin's Healing Effect on Motor Impairment in Rotenone-toxified Rodents.

BACKGROUND: Parkinson's disease is an illness marked by a gradual mitigation of dopamine neurons within the substantia nigra, which eventually leads to a deficiency of dopamine that further gives rise to mobility as well as cognitive impairments. Through long-established traditions, a wide array of Traditional Chinese Medicines (TCM) have undergone testing and are employed to avoid neurodegenerative disorders. Plumbagin is the primary active component of a medication called Baihua Dan or Plumbago zeylanica L., which is clinically used in China. OBJECTIVES: This study investigated plumbagin-induced alterations in a Parkinson's disease rat model instigated by subcutaneous rotenone injection. METHODS: Male rats were administered subcutaneous injections of rotenone at a dosage of 1.5 mg/kg, followed by the treatment with varying doses of plumbagin (10, 20, and 40 mg/kg) through the oral route. The rats underwent various motor ability tests, including the actophotometer, rotarod, open field, beam walk, gait evaluation, ability to grip, and catalepsy bar tests. Furthermore, the brain dopamine level was then estimated for the extracted tissues. Also, through molecular docking, the binding effectiveness of plumbagin was assessed for human MAO-B. After that, plumbagin was put through 100 ns of molecular dynamic simulations to examine the stability of its conformational binding to the target protein. Furthermore, ADMET tests were used to verify Plumbagin's druggability. RESULTS: Plumbagin was found to alleviate rotenone-induced motor abnormalities and restore brain dopamine levels. Furthermore, plumbagin showed excellent interactions with MAO-B (monoamine oxidase-B) when compared with selegiline (a standard drug for Parkinson's disease). CONCLUSION: These findings underscore the potential therapeutic efficacy of plumbagin in mitigating behavioural deficits in rotenone-induced rodents. Considering this, plumbagin might be a feasible pharmacological strategy for the control of rotenone-triggered behavioural impairment in rats (in vivo), and it might display interesting interactions with MAO-B (in silico).

Beyond insulin: The Intriguing role of GLP-1 in Parkinson's disease.

GLP-1 (Glucagon-like peptide 1) serves as both a peptide hormone and a growth factor, is released upon nutrient intake and contributes to insulin secretion stimulated by glucose levels. Also, GLP-1 is synthesized within several brain areas and plays a vital function in providing neuroprotection and reducing inflammation through the activation of the GLP-1 receptor. Parkinson's Disease (PD) is a neurodegenerative illness that worsens with time and is defined by considerable morbidity. Presently, there are few pharmaceutical choices available, and none of the existing therapies are capable of modifying the course of the disease. There is a suggestion that type 2 diabetes mellitus (T2DM) could increase the risk of PD, and the presence of both conditions concurrently might exacerbate PD symptoms and hasten neurodegeneration. GLP-1 receptor (GLP-1R) agonists exhibit numerous implications like enhancement of glucose-dependent insulin release and biosynthesis, suppression of glucagon secretion and gastric emptying. Also, some GLP-1R agonists have received clinical approval for the management of T2DM. Moreover, the use of GLP-1R agonists has demonstrated counter-inflammatory, neurotrophic, and neuroprotective actions in various preclinical models of neurodegenerative disorders. Considering the significant amount of evidence backing the potential of GLP-1R agonists to protect the nervous system across different research settings, this article delves into examining the hopeful prospect of GLP-1R agonists as a treatment option for PD. This review sheds light on combined neuroprotective benefits of GLP-1R agonists and the possible mechanisms driving the protective effects on the PD brain, through the collection of data from various preclinical and clinical investigations.

The Neuro-Healing Frontier: Alpha-Mangostin's Potential in Alzheimer's and Parkinson's Treatment.

Neurodegenerative disorders represent a set of advancing, severe, and incapacitating conditions impacting millions globally, with a rising prevalence. Despite concerted efforts and an enhanced understanding of the intricate pathophysiology of neurodegeneration, the quest for effective treatments remains unfulfilled. Consequently, there exists a pressing clinical necessity for the exploration of innovative therapeutic approaches. Alpha-mangostin has exhibited beneficial effects in alleviating the severity of neurodegenerative disorders, primarily attributed to its antioxidant properties. Alpha-mangostin showcases diverse pharmacological effects, encompassing anti-inflammatory, anti-tumour, and antioxidant effects. Consequently, it has surfaced as a promising remedy with both prophylactic and restorative impacts on various neurodegenerative ailments. Recent research has illuminated the therapeutic targets of alpha-mangostin, suggesting its potential utility in addressing neurodegeneration. This review showcases the neuroprotective effects of alpha-mangostin. Drawing from numerous preliminary studies and taking into account the compound's remedial effects, the primary focus is on its role as a health-giving compound for the therapy of diseases associated with the degeneration of the nervous system. Given the substantial evidence supporting its efficacy in various experimental models, this review advocates for further investigations, with a special highlight on elucidating neuroprotective mechanisms and conducting clinical trials to validate its effectiveness in managing Alzheimer's disease as well as Parkinson's disease.

Ferroptosis and circular RNAs: new horizons in cancer therapy.

Cancer poses intricate challenges to treatment due to its complexity and diversity. Ferroptosis and circular RNAs (circRNAs) are emerging as innovative therapeutic avenues amid the evolving landscape of cancer therapy. Extensive investigations into circRNAs reveal their diverse roles, ranging from molecular regulators to pivotal influencers of ferroptosis in cancer cell lines. The results underscore the significance of circRNAs in modulating molecular pathways that impact crucial aspects of cancer development, including cell survival, proliferation, and metastasis. A detailed analysis delineates these pathways, shedding light on the molecular mechanisms through which circRNAs influence ferroptosis. Building upon recent experimental findings, the study evaluates the therapeutic potential of targeting circRNAs to induce ferroptosis. By identifying specific circRNAs associated with the etiology of cancer, this analysis paves the way for the development of targeted therapeutics that exploit vulnerabilities in cancer cells. This review consolidates the existing understanding of ferroptosis and circRNAs, emphasizing their role in cancer therapy and providing impetus for ongoing research in this dynamic field. See also the graphical abstract(Fig. 1).

Revealing the Curative Possibilities: A Comprehensive Exploration of Caffeic Acid.

Caffeic acid, a phenolic compound of the hydroxycinnamic acid family, is abundant in various plant-based foods, such as fruits, vegetables, and coffee, alongside other biologically active compounds. Recognizing its potential to address various health issues and its widespread presence in commonly consumed foods underscores the importance of comprehending and harnessing the benefits of caffeic acid for human nutrition and well-being. This versatile substance, characterized by acrylic and phenolic functional groups, plays a pivotal role in the food and pharmaceutical industries. Furthermore, a detailed exploration of its pharmacokinetic properties, absorption, distribution, metabolism, and excretion enhances our understanding of how the human body processes it. Functioning as a precursor for essential compounds, caffeic acid contributes to formulations with notable anti-inflammatory, antiviral, anti-cancer, anti-diabetic, antibacterial, neuroprotective, and hepatoprotective qualities. Its current applications in treating Parkinson's and Alzheimer's disease underscore its therapeutic significance. This comprehensive analysis sheds light on caffeic acid's importance, showcasing its diverse applications across various domains and paving the way for further research and development to fully unlock its therapeutic potential. In conclusion, caffeic acid emerges as a bioactive substance with a broad spectrum of pharmacological properties, suggesting its potential utility in diverse therapeutic contexts. The comprehensive information provided in this article serves as a foundation for further research and learning regarding the various ways that caffeic acid supports human health.

Unveiling myricetin's pharmacological potency: A comprehensive exploration of the molecular pathways with special focus on PI3K/AKT and Nrf2 signaling.

Myricetin can be found in the traditional Chinese medicinal plant, Myrica rubra. Myricetin is a flavonoid that is present in many vegetables, fruits, and plants and is considered to have strong antioxidant properties as well as a wide range of therapeutic applications. Growing interest has been piqued by its classification as a polyphenolic molecule because of its potential therapeutic benefits in both the prevention and management of numerous medical conditions. To clarify myricetin's traditional medical uses, modern research has investigated various pharmacological effects such as antioxidant, anticancer, anti-inflammation, antiviral, antidiabetic, immunomodulation, and antineurodegenerative effects. Myricetin shows promise as a nutritional flavonol that could be beneficial in the prevention and mitigation of prevalent health conditions like diabetes, cognitive decline, and various types of cancer in humans. The findings included in this study indicate that myricetin has a great deal of promise for application in the formulation of medicinal products and nutritional supplements since it affects several enzyme activities and alters inflammatory markers. However, comprehensive preclinical studies and research studies are necessary to lay the groundwork for assessing myricetin's possible effectiveness in treating these long-term ailments. This review summarizes both in vivo and in vitro studies investigating myricetin's possible interactions through the nuclear factor-E2-related factor 2 (Nrf2) as well as PI3K (phosphatidylinositol 3-kinase)/AKT (protein kinase B) signaling pathways in an attempt to clarify the compound's possible clinical applicability across a range of disorders.

The impact of formaldehyde exposure on lung inflammatory disorders: Insights into asthma, bronchitis, and pulmonary fibrosis.

Lung inflammatory disorders are a major global health burden, impacting millions of people and raising rates of morbidity and death across many demographic groups. An industrial chemical and common environmental contaminant, formaldehyde (FA) presents serious health concerns to the respiratory system, including the onset and aggravation of lung inflammatory disorders. Epidemiological studies have shown significant associations between FA exposure levels and the incidence and severity of several respiratory diseases. FA causes inflammation in the respiratory tract via immunological activation, oxidative stress, and airway remodelling, aggravating pre-existing pulmonary inflammation and compromising lung function. Additionally, FA functions as a respiratory sensitizer, causing allergic responses and hypersensitivity pneumonitis in sensitive people. Understanding the complicated processes behind formaldehyde-induced lung inflammation is critical for directing targeted strategies aimed at minimizing environmental exposures and alleviating the burden of formaldehyde-related lung illnesses on global respiratory health. This abstract explores the intricate relationship between FA exposure and lung inflammatory diseases, including asthma, bronchitis, allergic inflammation, lung injury and pulmonary fibrosis.

Exploring ncRNA-mediated regulation of EGFR signalling in glioblastoma: From mechanisms to therapeutics.

Glioblastoma (GBM) is the most prevalent and deadly primary brain tumor type, with a discouragingly low survival rate and few effective treatments. An important function of the EGFR signalling pathway in the development of GBM is to affect tumor proliferation, persistence, and treatment resistance. Advances in molecular biology in the last several years have shown how important ncRNAs are for controlling a wide range of biological activities, including cancer progression and development. NcRNAs have become important post-transcriptional regulators of gene expression, and they may affect the EGFR pathway by either directly targeting EGFR or by modifying important transcription factors and downstream signalling molecules. The EGFR pathway is aberrantly activated in response to the dysregulation of certain ncRNAs, which has been linked to GBM carcinogenesis, treatment resistance, and unfavourable patient outcomes. We review the literature on miRNAs, circRNAs and lncRNAs that are implicated in the regulation of EGFR signalling in GBM, discussing their mechanisms of action, interactions with the signalling pathway, and implications for GBM therapy. Furthermore, we explore the potential of ncRNA-based strategies to overcome resistance to EGFR-targeted therapies, including the use of ncRNA mimics or inhibitors to modulate the activity of key regulators within the pathway.

Unraveling Amentoflavone's Therapeutic Potential in Alzheimer's Disease: A Preclinical Assessment.

Alzheimer's disease is one of the neurodegenerative diseases which causes cognition deficit. There are currently few medications available to treat Alzheimer's disease, even though researchers have devoted a great deal of time studying the condition and offering many benefits. Thus, only a few drugs are available for the treatment of Alzheimer's disease. Amentoflavone is a dietary component found in many plants and herbs that has several health advantages. Amentoflavone has demonstrated strong protective benefits against a range of brain illnesses in preclinical trials, most frequently in Alzheimer's disease. Amentoflavone, a biflavonoid, can be identified in a variety of herbs upon isolation. Considering the beneficial properties of this compound, this review emphasizes the pharmacological effects and botanical sources of amentoflavone, as well as the compound's benefits and possible applications in the treatment of Alzheimer's disorders.

Role of Nutraceuticals in Treating Erectile Dysfunction via Inhibition of Phosphodiesterase-5 Enzyme: A Mini Review.

Erectile Dysfunction (ED) is a prevalent sexual health condition affecting a significant portion of the male population worldwide. The conventional therapeutic approaches for ED often involve the use of pharmaceutical agents targeting the phosphodiesterase-5 (PDE5) enzyme. Currently, treatment with PDE-5 inhibitors is the standard approach for ED, and four PDE-5 inhibitors, namely sildenafil, vardenafil, tadalafil, and avanafil, are in use. However, these pharmaceutical interventions may be associated with adverse effects and limitations. As a result, there has been a growing interest in exploring alternative and complementary treatment options for ED, such as nutraceuticals, which are bioactive compounds derived from natural sources. Nutraceuticals, which include vitamins, minerals, herbs, and other dietary supplements, have gained popularity for their potential health benefits. Certain nutraceuticals have demonstrated the ability to modulate various physiological pathways, including those involved in erectile function. A notable mechanism of action is the inhibition of the PDE5 enzyme, which plays a pivotal role in the regulation of cGMP levels. By inhibiting PDE5, nutraceuticals can promote the accumulation of cGMP, leading to enhanced penile blood flow and improved erectile function. A comprehensive analysis of the literature showcases various nutraceutical agents, including plant-derived compounds like flavonoids, polyphenols, and amino acids which have exhibited PDE5 inhibitory effects. Mechanistic insights into their action involve modulation of NO release, cGMP elevation, and relaxation of penile smooth muscles, all critical factors for achieving and sustaining erections. This review focuses on elucidating the role of nutraceuticals in treating erectile dysfunction through the inhibition of the PDE5 enzyme.

Unraveling NEAT1's complex role in lung cancer biology: a comprehensive review.

This review delves into the pivotal role of the long non-coding RNA NEAT1 in cancer biology, particularly in lung cancer (LC). It emphasizes NEAT1's unique subcellular localization and active involvement in gene regulation and chromatin remodeling. The review highlights NEAT1's impact on LC development and progression, including cell processes such as proliferation, migration, invasion, and resistance to therapy, positioning it as a potential diagnostic marker and therapeutic target. The complex web of NEAT1's regulatory interactions with proteins and microRNAs is explored, alongside challenges in targeting it therapeutically. The review concludes optimistically, suggesting future avenues for research and personalized LC therapies, shedding light on NEAT1's crucial role in LC. See also the Graphical abstract(Fig. 1).

Therapeutic Potential of Capsaicin in Various Neurodegenerative Diseases with Special Focus on Nrf2 Signaling.

Neurodegenerative disease is mainly characterized by the accumulation of misfolded proteins, contributing to mitochondrial impairments, increased production of proinflammatory cytokines and reactive oxygen species, and neuroinflammation resulting in synaptic loss and neuronal loss. These pathophysiological factors are a serious concern in the treatment of neurodegenerative diseases. Based on the symptoms of various neurodegenerative diseases, different treatments are available, but they have serious side effects and fail in clinical trials, too. Therefore, treatments for neurodegenerative diseases are still a challenge at present. Thus, it is important to study an alternative option. Capsaicin is a naturally occurring alkaloid found in capsicum. Besides the TRPV1 receptor activator in nociception, capsaicin showed a protective effect in brain-related disorders. Capsaicin also reduces the aggregation of misfolded proteins, improves mitochondrial function, and decreases ROS generation. Its antioxidant role is due to increased expression of an nrf2-mediated signaling pathway. Nrf2 is a nuclear erythroid 2-related factor, a transcription factor, which has a crucial role in maintaining the normal function of mitochondria and the cellular defense system against oxidative stress. Intriguingly, Nrf2 mediated pathway improved the upregulation of antioxidant genes and inhibition of microglial-induced inflammation, improved mitochondrial resilience and functions, leading to decreased ROS in neurodegenerative conditions, suggesting that Nrf2 activation could be a better therapeutic approach to target pathophysiology of neurodegenerative disease. Therefore, the present review has evaluated the potential role of capsaicin as a pharmacological agent for the treatment and management of various neurodegenerative diseases via the Nrf2-mediated signaling pathway.

Exendin-4: A potential therapeutic strategy for Alzheimer's disease and Parkinson's disease.

Neurodegenerative disorders, which affect millions worldwide, are marked by a steady decline of neurons that are selectively susceptible. Due to the complex pathological processes underlying neurodegeneration, at present, there is no viable therapy available for neurodegenerative disorders. Consequently, the establishment of a novel therapeutic approach for such conditions is a clinical void that remains. The potential significance of various peptides as neuroprotective interventions for neurodegenerative disorders is gaining increasing attention. In the past few years, there has been growing scientific interest in glucagon-like peptide-1 receptor agonists due to their claimed neuroprotective effects. Exendin-4 is a glucagon-like peptide-1 receptor agonist that is known to possess anti-diabetic effects and does not degrade for hours, making it a superior candidate for such disorders. Moreover, exendin-4's neuroprotective effects have been reported in several preclinical studies. Exendin-4's diverse therapeutic targets suggest its potential therapeutic uses in neurodegenerative ailments like Alzheimer's disease and Parkinson's disease and have garnered an increasing amount of attention. Given the substantial body of evidence supporting the neuroprotective potential of exendin-4 in various research models, this article is dedicated to exploring the promising role of exendin-4 as a therapeutic agent for the treatment and management of Alzheimer's disease and Parkinson's disease. This review draws insights from the findings of numerous preclinical and clinical studies to highlight the collective neuroprotective advantages of exendin-4 and the potential mechanisms that underlie its neuroprotective effects.

Luteolin: Nature's promising warrior against Alzheimer's and Parkinson's disease.

Neurodegenerative disorders (NDs) are defined as the slow loss of a group of neurons that are particularly sensitive. Due to the intricate pathophysiological processes underlying neurodegeneration, no cure exists for these conditions despite the extensive research and advances in our knowledge of the onset and course of NDs. Hence, there is a medical need for the creation of a novel therapeutic approach for NDs. By focusing on numerous signaling pathways, some natural substances derived from medicinal herbs and foods have demonstrated potent activity in treating various NDs. In this context, flavonoids have recently attracted increased popularity and research attention because of their alleged beneficial effects on health. By acting as antioxidant substances, nutritional supplements made up of flavonoids have been found to lessen the extent of NDs like Alzheimer's disease (AD) and Parkinson's disease (PD). Luteolin is a flavone that possesses potent antioxidant and anti-inflammatory properties. As a consequence, luteolin has emerged as an option for treatment with therapeutic effects on many brain disorders. More research has focused on luteolin's diverse biological targets as well as diverse signaling pathways, implying its potential medicinal properties in several NDs. This review emphasizes the possible use of luteolin as a drug of choice for the treatment as well as the management of AD and PD. In addition, this review recommends that further research should be carried out on luteolin as a potential treatment for AD and PD alongside a focus on mechanisms and clinical studies.

Role of Alpha-7-Nicotinic Acetylcholine Receptor in Alzheimer's Disease.

Alzheimer's disease (AD) is a neurodegenerative disorder affecting millions worldwide. One of the leading hypotheses for the underlying cause of AD is a reduction in nicotinic receptor levels in the brain. Among the nicotinic receptors, the alpha-7-nicotinic acetylcholine receptor (α7nAChR) has received particular attention due to its involvement in cognitive function.α7nAChR is a ligand-gated ion channel that is primarily found in the hippocampus and prefrontal cortex, areas of the brain responsible for learning, memory, and attention. Studies have shown that α7nAChR dysfunction is a key contributor to the pathogenesis of AD. The receptor is involved in regulating amyloidbeta (Aß) production, a hallmark of AD pathology. Many drugs have been investigated as α7nAChR agonists or allosteric modulators to improve cognitive deficits in AD. Clinical studies have shown promising results with α7nAChR agonists, including improved memory and cognitive function. Although several studies have shown the significance of the α7 nAChR in AD, little is known about its function in AD pathogenesis. As a result, in this review, we have outlined the basic information of the α7 nAChR's structure, functions, cellular responses to its activation, and its role in AD's pathogenesis.