Nicotine via alpha7-nicotinic receptor induces ACE2 overexpression in Human Bronchial Epithelial Cells (HBEpC)

Nowadays, tobacco smoking is the cause of ~5–6 million deaths per year, counting 31% and 6% of all cancer deaths (affecting 18 different organs) in middle-aged men and women, respectively. Nicotine is the addictive component of tobacco acting on neuronal nicotinic receptors (nAChR). Functional nAChR, are also present on endothelial, haematological and epithelial cells. Although nicotine itself is regularly not referred to as a carcinogen, there is an ongoing debate whether nicotine functions as a ‘tumour promoter’. Nicotine, with its specific binding to nAChR, deregulates essential biological processes like regulation of cell proliferation, apoptosis, migration, invasion, angiogenesis, inflammation and cell-mediated immunity in a wide variety of cells including foetal (regulation of development), embryonic and adult stem cells, adult tissues as well as cancer cells. Nicotine seems involved in fundamental aspects of the biology of malignant diseases, as well as of neurodegeneration. Investigating the biological effects of nicotine may provide new tools for therapeutic interventions and for the understanding of neurodegenerative diseases and tumour biology.

Nicotine, the primary psychoactive agent in tobacco leaves, has led to the widespread use of tobacco, with over one billion smokers globally. This article provides a historical overview of tobacco and discusses tobacco dependence, as well as the biological effects induced by nicotine on mammalian cells. Nicotine induces various biological effects, such as neoangiogenesis, cell division, and proliferation, and it affects neural and non-neural cells through specific pathways downstream of nicotinic receptors (nAChRs). Specific effects mediated by α7 nAChRs are highlighted. Nicotine is highly addictive and hazardous. Public health initiatives should prioritize combating smoking and its associated risks. Understanding nicotine’s complex biological effects is essential for comprehensive research and informed health policies. While potential links between nicotine and COVID-19 severity warrant further investigation, smoking remains a significant cause of morbidity and mortality globally. Effective public health strategies are vital to promote healthier lifestyles.

The etiopathology of Alzheimer’s disease (AD) is extremely complex and heterogeneous, often associated with comorbidities. As a result it may be unlikely that AD may be mitigated by drug acting on a single specific target. The current tendency in drug design and discovery in AD is the rational design or “serendipitous” discovery of new drug entities challenging multiple targets. Since two of the presently approved drugs for AD are based on natural products (galantamine and the physostigmine-derivative rivastigmine), many plants are now under investigation as a potential source of new drugs. Multifunctional drugs often have their origin in natural sources. This review is limited to plant chemicals having different targets with actual (galantamine) or promising (drugs from Crocus sativus, Ginkgo biloba, Salvia species, and Huperzia serrata) clinical evidence in people with dementia or AD.

Alzheimer’s disease (AD) is a multifactorial neurodegenerative disorder. Current approved drugs may only ameliorate symptoms in a restricted number of patients and for a restricted period of time. Currently, there is a translational research challenge into identifying the new effective drugs and their respective new therapeutic targets in AD and other neurodegenerative disorders. In this review, selected examples of marine-derived compounds in neurodegeneration, specifically in AD field are reported. The emphasis has been done on compounds and their possible relevant biological activities. The proposed drug development paradigm and current hypotheses should be accurately investigated in the future of AD therapy directions although taking into account successful examples of such approach represented by Cytarabine, Trabectedin, Eribulin and Ziconotide. We review a complexity of the translational research for such a development of new therapies for AD. Bryostatin is a prominent candidate for the therapy of AD and other types of dementia in humans.

Background: Dietary habits influenced by lifestyle and cultural factors play a critical role in health by modulating oxidative stress and inflammation. While diets offer significant benefits, they may also pose risks, such as nutrient deficiencies, emphasizing the need for a balanced approach. Exploring Mediterranean and plant-based diet effects on oxidative stress and inflammation biomarkers may help improve health outcomes and disease prevention strategies. Methods: This study analyzed 65 studies following PRISMA guidelines to evaluate the effects of Mediterranean and plant-based diets on biomarkers of oxidative stress and inflammation in healthy individuals. Results: The Mediterranean diet was weakly associated with reductions in oxidative stress markers, including MDA (ROM: 0.80; 95% CI: 0.57–1.13; p = 0.2092) and 8OHdG (ROM: 0.81; 95% CI: 0.59–1.11; p = 0.1847), as well as inflammation markers such as CRP (ROM: 0.72; 95% CI: 0.42–1.23; p = 0.1545) and IL-6 (ROM: 1.23; 95% CI: 0.97–1.55; p = 0.08). The vegetarian diet significantly reduced CRP (ROM: 0.82; 95% CI: 0.69–0.98; p = 0.0297), while the vegan diet showed a borderline reduction (ROM: 0.81; 95% CI: 0.56–1.17; p = 0.2544), suggesting lower systemic inflammation compared to omnivorous diets. Conclusions: Although all three diets demonstrate potential in reducing oxidative stress and inflammation, the antioxidant effects—especially for the Mediterranean diet—are lower than anticipated, indicating alternative mechanisms. Further research is essential to confirm these findings and clarify the underlying mechanisms to enhance preventive health strategies.