Air pollution is a critical global issue with extensive implications beyond respiratory health, significantly affecting neurological and psychiatric disorders. Emerging evidence establishes a link between exposure to fine particulate matter (PM < 2.5 µm), sulfur dioxide (SO2), and nitrogen dioxide (NO2) and heightened risks of dementia, Alzheimer\'s disease, schizophrenia, ADHD, stroke, Parkinson\'s disease, and multiple sclerosis. Mechanistic pathways include neuroinflammation, oxidative stress, microglial activation, cerebrovascular dysfunction, and blood-brain barrier disruption. Epidemiological studies indicate increased susceptibility among urban residents, particularly men, middle-aged individuals, and married persons, to the mental health impacts of air pollution. Additionally, socioeconomic factors, such as GDP per capita, access to health resources, green spaces, and sports facilities, modulate these health outcomes. Addressing this public health challenge necessitates stricter industrial emission controls, sustainable agricultural practices, promotion of cleaner energy sources, and incorporation of pollution exposure history into clinical assessments. Enhanced public awareness and interdisciplinary research are vital for mitigating the detrimental effects of air pollution on neurological and psychiatric health, ultimately striving for a cleaner and healthier environment for future generations.

Excessive oxidative stress triggers cerebrovascular and neurodegenerative diseases resulting in acute and chronic brain injury. However, the underlying mechanisms remain unknown. Levels of small heat shock protein B8 (HSPB8), which is highly expressed in the brain, are known to be significantly elevated in cerebral injury models. Exogenous HSPB8 protects the brain against mitochondrial damage. One potential mechanism underlying this protection is that HSPB8 overexpression alleviates the mitochondria-dependent pathways of apoptosis; mitochondrial biogenesis, fission, and mitophagy. Overexpression of HSPB8 may therefore have potential as a clinical therapy for cerebrovascular and neurodegenerative diseases. This review provides an overview of advances in the protective effects of HSPB8 against excessive cerebral oxidative stress, including the modulation of mitochondrial dysfunction and potent signaling pathways.

The microbiota-gut-brain axis (MGBA) represents a sophisticated communication network between the brain and the gut, involving immunological, endocrinological, and neural mediators. This bidirectional interaction is facilitated through the vagus nerve, sympathetic and parasympathetic fibers, and is regulated by the hypothalamic-pituitary-adrenal (HPA) axis. Evidence shows that alterations in gut microbiota composition, or dysbiosis, significantly impact neurological disorders (NDs) like anxiety, depression, autism, Parkinson\'s disease (PD), and Alzheimer\'s disease (AD). Dysbiosis can affect the central nervous system (CNS) via neuroinflammation and microglial activation, highlighting the importance of the microbiota-gut-brain axis (MGBA) in disease pathogenesis. The microbiota influences the immune system by modulating chemokines and cytokines, impacting neuronal health. Synbiotics have shown promise in treating NDs by enhancing cognitive function and reducing inflammation. The gut microbiota\'s role in producing neurotransmitters and neuroactive compounds, such as short-chain fatty acids (SCFAs), is critical for CNS homeostasis. Therapeutic interventions targeting the MGBA, including dietary modulation and synbiotic supplementation, offer potential benefits for managing neurodegenerative disorders. However, more in-depth clinical studies are necessary to fully understand and harness the therapeutic potential of the MGBA in neurological health and disease.

BACKGROUND: Brain age model, including estimated brain age and brain-predicted age difference (brain-PAD), has shown great potentials for serving as imaging markers for monitoring normal ageing, as well as for identifying the individuals in the pre-diagnostic phase of neurodegenerative diseases.
OBJECTIVE: This study aimed to investigate the brain age models in normal ageing and mild cognitive impairments (MCI) converters and their values in classifying MCI conversion.
METHODS: Pre-trained brain age model was constructed using the structural magnetic resonance imaging (MRI) data from the Cambridge Centre for Ageing and Neuroscience (Cam-CAN) project (N = 609). The tested brain age model was built using the baseline, 1-year and 3-year follow-up MRI data from normal ageing (NA) adults (n = 32) and MCI converters (n = 22) drew from the Open Access Series of Imaging Studies (OASIS-2). The quantitative measures of morphometry included total intracranial volume (TIV), gray matter volume (GMV) and cortical thickness. Brain age models were calculated based on the individual\'s morphometric features using the support vector machine (SVM) algorithm.
RESULTS: With comparable chronological age, MCI converters showed significant increased TIV-based (Baseline: P = 0.021; 1-year follow-up: P = 0.037; 3-year follow-up: P = 0.001) and left GMV-based brain age than NA adults at all time points. Higher brain-PAD scores were associated with worse global cognition. Acceptable classification performance of TIV-based (AUC = 0.698) and left GMV-based brain age (AUC = 0.703) was found, which could differentiate the MCI converters from NA adults at the baseline.
CONCLUSIONS: This is the first demonstration that MRI-informed brain age models exhibit feature-specific patterns. The greater GMV-based brain age observed in MCI converters may provide new evidence for identifying the individuals at the early stage of neurodegeneration. Our findings added value to existing quantitative imaging markers and might help to improve disease monitoring and accelerate personalized treatments in clinical practice.
Based on individual’s MRI scans, brain age model has shown great potentials for serving as imaging markers for monitoring normal ageing (NA), as well as for identifying the ones in the pre-diagnostic phase of age-related neurodegenerative diseases. In this study, we investigated the brain age models in normal ageing and mild cognitive impairments (MCI) converters and their values in classifying MCI conversion. Pre-trained brain age model was constructed using the quantitative measures of morphometry included total intracranial volume (TIV), gray matter volume (GMV) and cortical thickness. With comparable chronological age, MCI converters showed significant increased brain age than NA adults at all time points. Higher brain age were associated with worse global cognition. This is the first demonstration that MRI-informed brain age models exhibit feature-specific patterns. The greater GMV-based brain age observed in MCI converters may provide new evidence for identifying the individuals at the early stage of neurodegeneration. Our findings added value to existing quantitative imaging markers and might help to improve disease monitoring and accelerate personalized treatments in clinical practice.

Adult hippocampal neurogenesis (AHN) is affected by multiple factors, such as enriched environment, exercise, ageing, and neurodegenerative disorders. Neurodegenerative disorders can impair AHN, leading to progressive neuronal loss and cognitive decline. Compelling evidence suggests that individuals engaged in regular exercise exhibit higher production of proteins that are essential for AHN and memory. Interestingly, specific molecules that mediate the effects of exercise have shown effectiveness in promoting AHN and cognition in different transgenic animal models. Despite these advancements, the precise mechanisms by which exercise mimetics induce AHN remain partially understood. Recently, some novel exercise molecules have been tested and the underlying mechanisms have been proposed, involving intercommunications between multiple organs such as muscle-brain crosstalk, liver-brain crosstalk, and gut-brain crosstalk. In this review, we will discuss the current evidence regarding the effects and potential mechanisms of exercise mimetics on AHN and cognition in various neurological disorders. Opportunities, challenges, and future directions in this research field are also discussed.

The spicy properties of foods are contributed by various spicy flavor substances (SFs) such as capsaicin, piperine, and allicin. Beyond their distinctive sensory characteristics, SFs also influence health conditions and numerous studies have associated spicy flavors with disease treatment. In this review, we enumerate different types of SFs and describe their role in food processing, with a specific emphasis on critically examining their influence on human wellness. Particularly, detailed insights into the mechanisms through which SFs enhance physiological balance and alleviate neurological diseases are provided, and a systematic analysis of the significance of transient receptor potential vanilloid type-1 (TRPV1) in regulating metabolism and nervous system homeostasis is presented. Moreover, enhancing the accessibility and utilization of SFs can potentially amplify the physiological effects. This review aims to provide compelling evidence for the integration of food flavor and human health.

Exposure to neurotoxic and heavy metals (Pb2+, As3+, Mn2+, Cd2+, etc) has increased over time and has shown to negatively affect brain health. Heavy metals can cross the blood brain barrier (BBB) in various ways including receptor or carrier-mediated transport, passive diffusion, or transport via gaps in the endothelial cells of the brain. In high concentrations, these metals have been shown to cause structural and functional impairment to the BBB, by inducing oxidative stress, ion dyshomeostasis, tight junction (TJ) loss, astrocyte/pericyte damage and interference of gap junctions. The structural and functional impairment of the BBB results in increased BBB permeability, which ultimately leads to accumulation of these heavy metals in the brain and their subsequent toxicity. As a result of these effects, heavy metals are correlated with various neurological disorders. The pathological effects of these heavy metals can be effectively mitigated via chelation. In addition, it is possible to treat the associated disorders by counteracting the molecular mechanisms associated with the brain and BBB impairment.

Neutrophil extracellular traps released by neutrophils are web-like DNA structures adhered to granulin proteins with bactericidal activity and can be an important mechanism for preventing pathogen dissemination or eliminating microorganisms. However, they also play important roles in diseases of other systems, such as the central nervous system. We tracked the latest advances and performed a review based on published original and review articles related to neutrophil extracellular traps and neurological diseases. Generally, neutrophils barely penetrate the blood-brain barrier into the brain parenchyma, but when pathological changes such as infection, trauma, or neurodegeneration occur, neutrophils rapidly infiltrate the central nervous system to exert their defensive effects. However, neutrophils may adversely affect the host when they uncontrollably release neutrophil extracellular traps upon persistent neuroinflammation. This review focused on recent advances in understanding the mechanisms and effects of neutrophil extracellular traps release in neurological diseases, and we also discuss the role of molecules that regulate neutrophil extracellular traps release in anticipation of clinical applications in neurological diseases.

Huntingtin-associated protein 1 (HAP1) was the first protein discovered to interact with huntingtin. Besides brain, HAP1 is also expressed in the spinal cord, dorsal root ganglion, endocrine, and digestive systems. HAP1 has diverse functions involving in vesicular transport, receptor recycling, gene transcription, and signal transduction. HAP1 is strongly linked to several neurological diseases, including Huntington\'s disease, Alzheimer\'s disease, epilepsy, ischemic stroke, and depression. In addition, HAP1 has been proved to participate in cancers and diabetes mellitus. This article provides an overview of HAP1 regarding the tissue distribution, cell localization, functions, and offers fresh perspectives to investigate its role in diseases.

BACKGROUND: While increased neurofilament light chain (NfL) in serum concentrations are linked to the progression of several neurological conditions, their distribution and implications within the general adult population remain largely unexplored. The current research aims to clarify the relationship between serum NfL levels and neurological disorders in a broad and representative population sample.
METHODS: We utilized information gathered from 1751 adults involved in the 2013-2014 cycle of the National Health and Nutrition Examination Survey . Our analytical approach encompassed logistic regression, smoothed curve fitting, and subgroup analyses to identify potential correlations between serum NfL levels and neurological conditions, such as depression, severe hearing and visual impairments, stroke, subjective memory deficits, and sleep problems.
RESULTS: After adjusting for all confounders, we found that higher serum NfL levels were significantly associated with increased risks of depression, stroke, subjective memory deficits, and longer sleep duration (p < 0.05). Subgroup analyses supported these findings. Additionally, BMI significantly influenced the relationship between serum NfL levels and long-term subjective memory decline.
CONCLUSIONS: Our research shows that higher serum NfL levels are strongly related to an elevated risk for several neurological disorders. These findings highlight the role of serum NfL serving as a critical marker for early detection and monitoring of neurological conditions, emphasizing its importance in both clinical and public health settings.