The Impact of Chemical Toxicants and Air Pollutants on Neurodegenerative Disorders and Their Underlying Potential Mechanisms: A Literature Review.

Cell death regulation is one of the important features that underlies the health and diseased conditions. All major neurodegenerative and neurological disorders inclusive of cancers and neurodegeneration can widely be attributed to dysregulated cell death mechanisms. Millions of people worldwide suffer from neurological and neurodegenerative disorders such as Alzheimer's Disease (AD), Parkinson's Disease (PD), Amylotrophic Lateral Sclerosis (ALS), Huntington's Disease (HD), Multiple Sclerosis (MS) and Stroke (Sarkar et al., 2016; Narwal et al., 2024). A common underlying feature for all these conditions is neuronal cell death, which has been studied in great detail by researchers for understanding the "cause and the effect" of the symptoms (Singh, 2012). Current understanding gathered from different model organisms, organoid transplants and the in-vitro approaches points in the direction that the majority of neurodegenerative disorders are due to proteinopathies, which eventually result in neuronal cell death. This research topic emphasizes on the advancements in understanding the varied mechanisms underlying different types of cell death(s) during the course of neurodegenerative disorders. The collection advances the understanding and raises new questions to aid ongoing research across different model systems. Conservation of genetic machinery and amenability of various models to genetic manipulation helped address these questions in various animal models. We believe that this research topic enables researchers to develop detailed understanding of cell death mechanisms, unravel the gaps and missing links and identify the interconnecting pathways to discern neurodegenerative disorders to develop better therapies and management strategies. Cell death pathways in neurodegeneration Studies from invertebrate and mammalian models suggest that neurodegenerative disorders involving protein misfolding and aggregations such as AD, PD and ALS, are characterized by activation of various kinds of cell death pathways including apoptosis, autophagy, ferroptosis and necrosis (Rai and Bergmann, Li et al). Interestingly, interpreted factors, which are common neurodegeneration cascades from these models are production of ROS, mitochondrial dysfunction and disturbed immune response pathways. There are multiple studies which indicate connections between protein aggregation, ROS production leading to activation of inflammatory pathways involving different types of neuronal and non-neuronal cells (Deshpande et al, 2024). Abnormal iron homeostasis affects protein aggregations, leading to enhanced ROS production causing ferroptosis in case of PD. Studies from glia-neuron interactions have provided evidence for the role of glial cells in maintenance of iron homeostasis regulating dopaminergic neuronal loss (Li et al). Activation of glial cells results in activation of Nuclear Factor-Kappa-B (NF-kB) which causes upregulation of inflammatory molecules, thereby causing inflammation in neuronal tissues in conditions of neurodegeneration (Reviewed in Heneka et al, 2024). In addition to apoptosis, autophagy, ferroptosis, necrosis and pyroptosis have also been well documented in conditions of neurodegeneration and neurological conditions such as stroke (Rinald and Troy). Genetic as well as environmental factors have been extensively studied which can cause neurodegenerative and neurological diseases (Banerjee et al, 2022; Iyer et al, 2024; Yogi et al, 2024). Altered nucleic acid metabolism has also been studied in context to neurodegenerative disorders (Chimata et al, 2024; Singh et al, 2025). Interestingly, three stranded non-canonical DNA-RNA hybrid templates have also been identified to be involved in mediating cellular damage enhancing pathogenesis of several human diseases, including neurodegeneration mediated in ALS, ataxia and spinal muscular atrophy (Liu et al). Different kinds of cell death regulate the progression of neurodegenerative and neurological disorders/injuries, it is noteworthy that modeling of different kinds of cell death in different model systems is crucial to develop not only therapeutics, but also early diagnosis. We acknowledge the insights into cell death regulatory pathways developed from models including invertebrate models such as flies up-to mammalian systems, organoid transplants and patient samples. Articles presented in this section have highlighted various kinds of cell deaths which mediate neuronal loss in different conditions. It is evident that mechanisms involved in mediating neurodegenerative and neurological disorders are multifactorial; possibly due to different mechanisms which mediate neuronal injury and eventual loss. We believe that this collection will aid in advancing the understanding of the field of neurodegenerative disorders in order to develop better diagnostic and therapeutic measures in future.

Roles of pollution in the prevalence and exacerbations of allergic diseases in Asia

In the context of an ageing society neurodegenerative disease have become more and more frequent among humans. Opposing the benefits of a longer life, these diseases have thus triggered research on neurons and how they interact with each other. In vitro as well as in vivo experiments are comparably involved. Due to the complex mechanisms occurring at the neuronal level there is a need for developing suitable techniques. Such techniques are required to provide high resolution in several respects in order to track cellular properties: Fourier transform infrared spectroscopy (FTIR) along with high-brilliance synchrotron radiation matches the requirements of high spectral and spatial resolution for chemical distinction perfectly. We have investigated a rat model of Huntington's disease (HD) with synchrotron-assisted Fourier transform infrared microspectroscopy (SIRMS). Several neurodegenerative diseases, ranging from Alzheimer's to prion disease, have now been identified to be caused by proteins which auto-assemble into high molecular weight amyloid aggregates or fibrils. HD is related to abnormal polyglutamine (polyQ) repeats. Its symptoms are progressive deterioration of cognitive and motor functions, along with extensive loss of neurons. In our model, one brain hemisphere was infected with HD while keeping the second one as a control. The two types of matter in the striatum are affected in different manners: in neuron-rich gray matter exposed to the disease, a higher content of aggregated protein is detected, but no signs of cell death. In contrast, myelin-rich white matter did not show any aggregates, but surprisingly showed a significant increase in phosphorylation. We interpret this result as the activation of the cellular response to stress which leads in the end to cell death. The drastic changes in the white matter were detected in the case of multiple sclerosis. We have studied its animal model, the experimental autoimmune encephalomyelitis (EAE). EAE is characterized by heavy loss of the insulating lipid-layer, the myelin around axons. This has been clearly confirmed by SIRMS and FTIR. Analysis of spatially resolved maps by both unsupervised principal component analysis and chemical signatures showed additional features of EAE. Both studies indicate that SIRMS is a powerful tool of detecting complex chemical processes in biological tissue in a relatively easy way. In addition to nanometer spatial resolution, the photonic force microscope (PFM) provides microsecond temporal resolution. A PFM tracks the Brownian motion of micron-sized beads embedded in solutions. Thanks to the high resolutions, we can calculate velocity auto-correlation functions (vacf) of the beads that are extremely sensitive on the short-time scale. We found that they depend in solutions containing polymers on the mesh size. The narrower the polymer mesh size, the earlier perturbations occur in the bead's motion. Polymer solutions possess a very interesting feature which is their viscoelasticity. Based on the mean square displacements of the beads, the complex shear modulus is obtained describing in a frequency-dependent manner viscosity and elasticity. In this way we could distinguish different polymers and also a pathologically relevant fibril: α-synuclein involved in Parkinson's disease.

Air Pollution and Coronary Risk in Kidney Transplant Recipients

Pregnancy and early childhood are periods with high plasticity in neurological development. Environmental perturbations during these sensitive windows can have lifelong developmental consequences. This review summarizes key findings relevant to the effects of air pollution on neurological development. Mounting evidence suggests that exposure to air pollution, both during pregnancy and childhood, is associated with childhood developmental outcomes ranging from changes in brain structures to subclinical deficits in developmental test scores, and, ultimately, developmental disorders such as attention-deficit/hyperactivity disorders or autism spectrum disorders. Although the biological mechanisms of effects remain to be elucidated, multiple pathways are probably involved and include oxidative stress, inflammation, and/or endocrine disruption. Given the alarming global increase in developmental disorders in recent years, and increased human exposures to pollution, it is critical to reduce personal and community-level exposures through tight collaboration of interdisciplinary and multi-level bodies including community partners, physicians, industry partners, policy makers, public health practitioners, and researchers. WHAT THIS PAPER ADDS: Exposure to air pollution is associated with a range of childhood developmental complications. Biological mechanisms may include oxidative stress, inflammation, and endocrine disruption.

Alzheimer disease (AD); Parkinson disease (PD); Huntington disease (HD); amyotrophic lateral sclerosis (ALS); neurofibrillary tangle (NFT); superoxide dismutase-1 (SOD1); programmed cell death (PCD).

The purpose of this study is to show the adverse effects of environmental pollutants on human health. Chapter 1 is an introduction to the subject. Chapter 2 focuses on glyphosate and glyphosate-based herbicides (GBHs) and their impact on the mammalian nervous system. Glyphosate is the active ingredient in GBHs, such as Roundup™, the most widely used herbicide worldwide. In addition to cancer and reproductive effects, glyphosate and GBHs have adverse effects on the brain and behavioral health and increase the risk of at least some serious neurological disorders. I reviewed scientific reports on the effects of glyphosate and GBHs on the mammalian nervous system; exposure to GBHs increases the risk of Parkinson's Disease and causes death of substantia nigra neurons. Roundup™ has also been linked to an increased risk of autism in some studies. Oxidative stress and mitochondrial dysfunction are the major mechanisms of action. Chapters 3 and 4 show the adverse effects of air pollution on human health and its association with respiratory diseases. Air pollution is of great concern due to the strong evidence that it causes an increased mortality and morbidity and contributes to climate change and negative human health impacts. Most research on air pollution and human disease has focused on the priority pollutants, especially particulates. However, volatile organic compounds (VOCs) are also major air pollutants, and the effects of inhalation of VOCs have been less studied. Exposure to VOCs like benzene, toluene, ethyl benzene, xylene (BTEX), and formaldehyde also have the potential to pose serious health risks. Many adverse health outcomes have been linked to VOCs, including cardiovascular disease, respiratory diseases, and asthma. There needs to be further research on the adverse effects of non-occupational exposures to VOCs on human health, as current results are inconclusive. The overarching objective of this project is to determine the degree to which exposure to VOCs from all sources and particularly from point sources affects human health. The exposure data comes from the US EPA National Emissions Inventory (NEI), a data set of air emissions and pollutants from point sources, as well as total exposure by county. This research project examines the rates of hospital emergency room (ER) visits for asthma, chronic obstructive pulmonary disease (COPD), acute lower respiratory disease, and acute upper respiratory diseases among patients who were exposed to higher concentrations of VOC air pollutants. Data on patients' ER visits come from the Statewide Planning and Research Cooperative System (SPARCS) database. The use of these datasets allows one to provide an indication of the risk of respiratory diseases caused by air pollutants, from all sources of pollution at the county level and at zip code levels in relation to point source emissions. This study shows that there is a higher risk of respiratory diseases among poor people; there is a strong association between air pollution and asthma attacks, and between smoking and COPD. These findings demonstrate that local VOCs pollution results in a small but significant contribution to the risk of respiratory disease-related ER visits.

Background: Environmental tax has been implemented by the government in response to the demands of the residents to control environmental pollution. However, a tax has a wide effect on many interacting aspects of the society. It remains unknown whether enacting an environmental tax for the government can improve the residents’ happiness. This study aimed to examine the impact of air and water pollution on residents’ happiness and evaluate whether an environmental tax can alleviate the impact of air and water pollution on residents’ happiness. Methods: Based on the 2015 Chinese General Social Survey Data, 28 provinces in China were divided into two categories according to their environmental tax rates: baseline-tax areas (n = 13) and high-tax areas (n = 15). The ordered probit model was used to analyze the impact of air and water pollution on the residents’ happiness in baseline-tax areas and high-tax areas, respectively. The Chow Test was used to test whether the impact of environmental pollution on happiness was different between baseline-tax areas and high-tax areas. Results: The impact of air pollution on residents’ happiness was statistically significant in the baseline-tax areas (coefficient −0.162, 95% confidence interval (CI) −0.239, −0.086, p < 0.001), but the significance was weakened in the high-tax areas (coefficient −0.030, 95% CI −0.060, 0.000, p = 0.051). The Chow Test showed that the absolute value of the regression coefficient in the baseline-tax areas was significantly higher than the value in the high-tax areas (F = 12.712, p < 0.001). Similarly, the impact of water pollution on residents’ happiness was statistically significant (coefficient −0.264, 95% CI −0.353, −0.174, p < 0.001) in the baseline-tax areas and in the high-tax areas (coefficient −0.063, 95% CI −0.091, −0.035, p < 0.001), but the Chow Test showed that the absolute value of the regression coefficient in the baseline-tax areas was significantly higher than the value in the high-tax areas (F = 13.758, p < 0.001). Conclusions: Both air and water pollution impair residents’ happiness. The present study shows for the first time that enacting an environmental tax significantly alleviates the negative effect of air and water pollution on residents’ happiness. The findings of the present study provide empirical evidence for the government to levy environmental tax.

Neurodegenerative diseases such as Alzheimer's disease (AD), Parkinson's disease (PD), Amyotrophic lateral sclerosis (ALS), Multiple sclerosis (MS), and Huntington's disease (HD) represent a growing global health challenge, especially with aging populations. Characterized by progressive neuronal loss, these diseases lead to cognitive, motor, and behavioral impairments, significantly impacting patients' quality of life. Current therapies largely address symptoms without halting disease progression, underscoring the need for innovative, disease-modifying treatments. Ginseng, a traditional herbal medicine with well-known adaptogenic and neuroprotective properties, has gained attention as a potential therapeutic agent for neurodegeneration. Rich in bioactive compounds called ginsenosides, ginseng exhibits antioxidant, anti-inflammatory, and anti-apoptotic effects, making it a promising candidate for addressing the complex pathology of neurodegenerative diseases. Recent studies demonstrate that ginsenosides modulate disease-related processes such as oxidative stress, protein aggregation, mitochondrial dysfunction, and inflammation. In AD models, ginsenosides have been shown to reduce amyloid-beta accumulation and tau hyperphosphorylation, while in PD, they help protect dopaminergic neurons and mitigate motor symptoms. Ginseng's effects in ALS, MS, and HD models include improving motor function, extending neuronal survival, and reducing cellular toxicity. This review provides a comprehensive overview of the neuroprotective mechanisms of ginseng, emphasizing its therapeutic potential across various neurodegenerative diseases and discussing future research directions for its integration into clinical practice.

The study of human movement and biomechanics forms an integral part of various clinical assessments and provides valuable information toward diagnosing neurodegenerative disorders where the motor symptoms predominate. Conventional gait and postural balance analysis techniques like force platforms, motion cameras, etc., are complex, expensive equipment requiring specialist operators, thereby posing a significant challenge toward translation to the clinics. The current manuscript presents an overview and relevant literature summarizing the umbrella of factors associated with neurodegenerative disorder management: from the pathogenesis and motor symptoms of commonly occurring disorders to current alternate practices toward its quantification and mitigation. This article reviews recent advances in technologies and methodologies for managing important neurodegenerative gait and balance disorders, emphasizing assessment and rehabilitation/assistance. The review predominantly focuses on the application of inertial sensors toward various facets of gait analysis, including event detection, spatiotemporal gait parameter measurement, estimation of joint kinematics, and postural balance analysis. In addition, the use of other sensing principles such as foot-force interaction measurement, electromyography techniques, electrogoniometers, force-myography, ultrasonic, piezoelectric, and microphone sensors has also been explored. The review also examined the commercially available wearable gait analysis systems. Additionally, a summary of recent progress in therapeutic approaches, viz., wearables, virtual reality (VR), and phytochemical compounds, has also been presented, explicitly targeting the neuro-motor and functional impairments associated with these disorders. Efforts toward therapeutic and functional rehabilitation through VR, wearables, and different phytochemical compounds are presented using recent examples of research across the commonly occurring neurodegenerative conditions [viz., Parkinson’s disease (PD), Alzheimer’s disease (AD), multiple sclerosis, Huntington’s disease (HD), and amyotrophic lateral sclerosis (ALS)]. Studies exploring the potential role of Phyto compounds in mitigating commonly associated neurodegenerative pathologies such as mitochondrial dysfunction, α-synuclein accumulation, imbalance of free radicals, etc., are also discussed in breadth. Parameters such as joint angles, plantar pressure, and muscle force can be measured using portable and wearable sensors like accelerometers, gyroscopes, footswitches, force sensors, etc. Kinetic foot insoles and inertial measurement tools are widely explored for studying kinematic and kinetic parameters associated with gait. With advanced correlation algorithms and extensive RCTs, such measurement techniques can be an effective clinical and home-based monitoring and rehabilitation tool for neuro-impaired gait. As evident from the present literature, although the vast majority of works reported are not clinically and extensively validated to derive a firm conclusion about the effectiveness of such techniques, wearable sensors present a promising impact toward dealing with neurodegenerative motor disorders.

Could Environmental Exposures Facilitate the Incidence of Addictive Behaviors?

Conservation organizations have most often focused on land-use change, climate change, and invasive species as prime threats to biodiversity conservation. Although air pollution is an acknowledged widespread problem, it is rarely considered in conservation planning or management. In this synthesis, the state of scientific knowledge on the effects of air pollution on plants and animals in the Northeastern and Mid-Atlantic regions of the United States is summarized. Four air pollutants (sulfur, nitrogen, ozone, and mercury) and eight ecosystem types ranging from estuaries to alpine tundra are considered. Effects of air pollution were identified, with varying levels of certainty, in all the ecosystem types examined. None of these ecosystem types is free of the impacts of air pollution, and most are affected by multiple pollutants. In aquatic ecosystems, effects of acidity, nitrogen, and mercury on organisms and biogeochemical processes are well documented. Air pollution causes or contributes to acidification of lakes, eutrophication of estuaries and coastal waters, and mercury bioaccumulation in aquatic food webs. In terrestrial ecosystems, the effects of air pollution on biogeochemical cycling are also very well documented, but the effects on most organisms and the interaction of air pollution with other stressors are less well understood. Nevertheless, there is strong evidence for effects of nitrogen deposition on plants in grasslands, alpine areas, and bogs, and for nitrogen effects on forest mycorrhizae. Soil acidification is widespread in forest ecosystems across the eastern United States and is likely to affect the composition and function of forests in acid-sensitive areas over the long term. Ozone is known to cause reductions in photosynthesis in many terrestrial plant species. For the most part, the effects of these pollutants are chronic, not acute, at the exposure levels common in the eastern United States. Mortality is often observed only at experimentally elevated exposure levels or in combination with other stresses such as drought, freezing, or pathogens. The notable exceptions are the acid/aluminum effects on aquatic organisms, which can be lethal at levels of acidity observed in many surface waters in the region. Although the effects are often subtle, they are important to biological conservation. Changes in species composition caused by terrestrial or aquatic acidification or eutrophication can propagate throughout the food webs to affect many organisms beyond those that are directly sensitive to the pollution. Likewise, sublethal doses of toxic pollutants may reduce the reproductive success of the affected organisms or make them more susceptible to potentially lethal pathogens. Many serious gaps in knowledge that warrant further research were identified. Among those gaps are the effects of acidification, ozone, and mercury on alpine systems, effects of nitrogen on species composition of forests, effects of mercury in terrestrial food webs, interactive effects of multiple pollutants, and interactions among air pollution and other environmental changes such as climate change and invasive species. These gaps in knowledge, coupled with the strong likelihood of impacts on ecosystems that have not been studied in the region, suggests that current knowledge underestimates the actual impact of air pollutants on biodiversity. Nonetheless, because known or likely impacts of air pollution on the biodiversity and function of natural ecosystems are widespread in the Northeast and Mid-Atlantic regions, the effects of air pollution should be considered in any long-term conservation strategy. It is recommended that ecologically relevant standards, such as "critical loads," be adopted for air pollutants and the importance of long-term monitoring of air pollution and its effects is emphasized.

Air pollution is one of the major causes of mortality and morbidity in the world today. World Health Organization (WHO) data show that almost all of the global population (99%) breathe air that exceeds WHO guideline limits and contains high levels of pollutants, with low- and middle-income countries suffering most from air pollution exposure. In China, the largest developing country, the poor air quality is primarily attributed to the rapid economic expansion the country experienced since the reform and opening-up in 1978, resulting in a drastic increase in coal-powered industrial production and electricity demand, as well as an exponential rise in private vehicles. Although there has been continuous air quality improvement following a series of stringent control policies, air pollution remains an important public health threat in China. The Global Burden of Disease Study estimated that in 2019, air pollution was responsible for 1.85 million deaths in China[1]. Meanwhile, non-communicable diseases (NCDs), such as cardiovascular disease and cancer, have placed much more disease burden on the population than ever[2]. It has been estimated that cardiovascular disease is now the leading cause of death in the Chinese population of adults 40 years of age and older, accounting for around 40% of total mortality. A growing body of human and animal evidence has led to a concern about the potential deleterious effects of ambient air pollution on the cardiovascular system[3,4]. For example, using the largest nationwide data in 272 Chinese cities, Chen et al. reported that a 10 μg/m3 increment of PM2.5 was associated with an increase of 0.27% in cardiovascular mortality. Similarly, in 652 cities of 24 countries, Liu et al. reported that an increase of 10 μg/m3 increment of PM2.5 was associated with increases of 0.36% in daily cardiovascular mortality[5]. The mixture of air pollutants may adversely affect the cardiovascular system directly and indirectly[6]. Direct effects may occur via agents that readily cross the pulmonary epithelium into the circulation, such as ultra-fine particles (UFPs), soluble constituents of particles (e.g., sulfate and nitrate), and gaseous pollutants (e.g., nitrogen oxides). Indirect effects may occur via induction of pulmonary inflammation and oxidative stress, leading to systemic inflammation and endothelial dysfunction. Although the adverse cardiovascular effects of air pollution have been documented in China, questions remain to be solved in human-based studies, especially for a stronger causal inference[7]. In this issue, we invited esteemed colleagues from some of the most reputable institutions in China and the United States, including Yale University, the Chinese Center for Disease Control and Prevention, Fudan University, and Chinese Academy of Medical Sciences and Peking Union Medical College to report their latest findings on air pollution and cardiovascular disorders. Their intriguing findings underscore the importance of understanding the health impacts of air pollution, particularly in China where the problem is especially severe due to rapid industrialization and urbanization. Ban et al. investigated the linear and non-linear patterns for the association between PM2.5 and acute incidence of myocardial infarction (MI) based on a multi-county registry dataset. They evaluated the reduction of premature MI incidence under different pollution control objectives in China[8]. This study provided valuable insights into the impact of PM2.5 on cardiovascular health on a national scale, and its findings can help inform policies aimed at reducing the burden of cardiovascular disease in China. Du et al. investigated the health effects of short-term exposure to PM2.5 from agricultural sources on acute MI onset using a nationwide database in China[9]. The study found that exposure to agricultural PM2.5 was associated with an increased risk of acute MI, highlighting the need for more research on estimating the adverse health effects of different air pollution sources. The study conducted by Jiang et al. explored the impacts of PM2.5 and PM2.5–10 on the onset of stable and unstable angina at an hourly temporal resolution, adjusting for key confounders[10]. They suggest that life-threatening cardiovascular disease risk from transient exposure to air pollution must be considered by healthcare professionals including cardiologists and patient caregivers to avoid negative cardiorespiratory outcomes. Finally, Zhou et al. reviewed available evidence quantifying the relationship between exposure to ambient gaseous and particulate air pollutants and cardiovascular symptoms[11]. The study found that exposure to air pollution was associated with a wide range of cardiovascular symptoms, including heart failure, arrhythmias, and hypertension. Although the findings above confirm that air pollution contributes to the cardiovascular disorders in China, several questions or challenges remain to be solved in human-based studies, especially for a stronger causal inference. Although some recent prospective cohort studies in China have examined the long-term effects of air pollution on cardiovascular mortality or morbidity[12], cohort studies are still lacking in examining a full spectrum of cardiometabolic diseases. Most Chinese studies on air pollution and cardiovascular health are observational in nature, thus limiting the power of causal inference. Accountability studies that evaluate long-term health benefits of clean air policies and intervention studies that reduce individual exposure may help to establish a causal relationship between air pollution and cardiovascular health[13]. The application of the difference-in-differences approach and randomized crossover design in intervention studies have been shown to further improve the causality[14]. Controlled-exposure human trials are particularly useful to establish the biological causation for the adverse cardiovascular effects of air pollution[15]. As research on the relationship between air pollution and cardiovascular health in the Chinese population continues to evolve, it is important to remember the many questions and challenges that remain. One area requiring further investigation is the lifetime course of cardiovascular damage effects, which could be addressed through prospective cohort studies. By following a large cohort of individuals over time, researchers can better understand how air pollution exposure affects the development and progression of cardiovascular diseases over the course of an individual's life. In addition to clarifying the long-term effects of air pollution on cardiovascular health, it is also important to examine the relevance of cumulative exposure. This requires not only tracking the levels of air pollution that individuals are exposed to over time but also considering how exposure to other risk factors, such as smoking, physical activities, green space, or a poor diet, may interact with air pollution exposure to affect cardiovascular health outcomes. By taking a more comprehensive approach to understanding the health impacts of air pollution, researchers can help to identify the most vulnerable populations and periods and develop more effective public health interventions to mitigate the negative health effects of air pollution. Another crucial area for future research is the investigation of genetic–environment interactions in relation to air pollution exposure and cardiovascular health. While genetic factors have been shown to play a role in the development of cardiovascular disease, their interaction with environmental factors such as air pollution is still poorly understood. By identifying genetic variations that may increase an individual's susceptibility to the negative health effects of air pollution, researchers can help to develop more personalized approaches to the prevention and treatment of cardiovascular diseases. Finally, it is important to establish the pathophysiologic link between air pollution and cardiometabolic diseases in the Chinese population. This requires identifying the specific mechanisms by which air pollution exposure leads to cardiovascular disease and understanding how these mechanisms may differ across different population subgroups. By gaining a more detailed understanding of the biological pathways that link air pollution exposure to cardiovascular disease, researchers can help to develop more targeted and effective interventions to mitigate the negative health effects of air pollution. Beyond these research priorities, there is clear evidence showing that climate change poses significant health risks to the population, and population health risks due to environmental factors under changing climate will become more severe in the future[16]. Air quality is closely linked to the earth's climate and ecosystems globally, as many of the air pollutants and greenhouse gases share the same sources (e.g., combustion of fossil fuels). Therefore, policies to reduce air pollution offer a win-win strategy for both climate and health, lowering the burden of disease attributable to air pollution, and contributing to the near- and long-term mitigation of climate change can be accomplished at the same time. Therefore, air pollution, climate change, and population health need to be considered simultaneously. Meanwhile, health risks from environmental factors will persist under climate change, and gaps in research evidence that may support population adaptation should be filled. In addition, innovative technologies and methodologies that may be applied to population health interventions should be developed. In summary, consideration of the health impacts and coping strategies of air pollution and climate change can help the government move forward towards sustainable development with appropriate urgency, reducing the disease burden and promoting a more healthy and sustainable future for all. CONFLICTS OF INTEREST STATEMENT Haidong Kan is an Editorial Board member of Cardiology Plus.

Psychopathology in Verified Huntington's Disease Gene Carriers

This review highlights the significance of adopting an anti-inflammatory diet for the prevention and treatment of neurodegenerative disorders and mental illnesses, focusing on Parkinson’s disease (PD), Huntington’s disease (HD), multiple sclerosis (MS), depression, schizophrenia, and bipolar disorder (BD). In PD a diet rich in antioxidants (e.g., vitamins C and E, beta-carotene) and the Mediterranean diet may reduce risk and improve symptoms. The gut microbiome also plays a role, with probiotics offering potential benefits by reducing inflammation and improving metabolic state. In HD, diets like the Mediterranean diet and ketogenic diet show promise in managing HD by reducing oxidative stress and improving quality of life. MS, benefits from an anti-inflammatory diet rich in fruits, vegetables, low-fat dairy, probiotics, and healthy fats. Depression, Schizophrenia and BD exacerbated by the COVID-19 pandemic, has been linked to inflammatory diets. Anti-inflammatory diets, such as the DASH and ketogenic diets, have shown potential in reducing depression severity. Omega-3 fatty acids, antioxidants, and the Mediterranean diet can improve symptoms and overall health outcomes by reducing inflammation. Methods: This review explores how diet and its elements impact inflammation associated with neurological diseases. It combines data from in vitro experiments, animal studies, and various research, offering a thorough assessment of the effectiveness of nutritional interventions in addressing neurodegenerative disorders. Systematic searches of credible databases such as PubMed and Google Scholar were conducted to include the most current and reliable literature. Conclusion: Anti-inflammatory diets offer a promising adjunct to traditional treatments for these neurodegenerative disorders and mental illnesses, emphasizing the need for further research to optimize dietary interventions and understand underlying mechanisms. Personalized nutrition strategies could enhance treatment efficacy and patient well-being.