Over the last several years, a growing body of evidence from anatomical, physiological, and functional neuroimaging studies has increasingly indicated that the cerebellum is actively involved in managing higher order cognitive functions and regulating emotional responses. It has become clear that when children experience congenital or acquired cerebellar lesions, these injuries can lead to a variety of cognitive and emotional disorders, manifesting in different combinations. This underscores the cerebellum\'s essential role not only throughout developmental stages but particularly in facilitating learning processes, highlighting its critical importance beyond its traditional association with motor control. Furthermore, the intricate neural circuits within the cerebellum are believed to contribute to the fine-tuning of motor actions and coordination but are also increasingly recognized for their involvement in cognitive processes such as attention, language, and problem solving. Recent research has highlighted the importance of cerebellar health and integrity for optimal functioning across various domains of the human experience.

UNASSIGNED: Air pollution is a significant contributor to morbidity and mortality globally and has been linked to an increased risk of dementia. Previous studies within the Betula cohort in Northern Sweden have demonstrated associations between air pollution and dementia, as well as distinctive metabolomic profiles in dementia patients compared to controls. This study aimed to investigate whether air pollution is associated with quantitative changes in metabolite levels within this cohort, and whether future dementia status would modify this association.
UNASSIGNED: Both short-term and long-term exposure to air pollution were evaluated using high spatial resolution models and measured data. Air pollution from vehicle exhaust and woodsmoke were analyzed separately. Metabolomic profiling was conducted on 321 participants, including 58 serum samples from dementia patients and a control group matched for age, sex, and education level, using nuclear magnetic resonance spectroscopy.
UNASSIGNED: No statistically significant associations were found between any metabolites and any measures of short-term or long-term exposure to air pollution. However, there were trends potentially suggesting associations between both long-term and short-term exposure to air pollution with lactate and glucose metabolites. Notably, these associations were observed despite the lack of correlation between long-term and short-term air pollution exposure in this cohort. There were also tendencies for associations between air pollution from woodsmoke to be more pronounced in participants that would later develop dementia, suggesting a potential effect depending on urban/rural factors.
UNASSIGNED: While no significant associations were found, the trends observed in the data suggest potential links between air pollution exposure and changes in lactate and glucose metabolites. These findings provide some new insights into the link between air pollution and metabolic markers in a low-exposure setting. However, addressing existing limitations is crucial to improve the robustness and applicability of future research in this area. The pronounced associations in participants who later developed dementia may indicate an influence of urban/rural factors, warranting further investigation.

Cadmium (Cd) induced neurotoxicity has become a growing concern due to its potential adverse effects on the Central Nervous System. Cd is a Heavy Metal (HM) that is released into the environment, through several industrial processes. It poses a risk to the health of the community by polluting air, water, and soil. Cd builds up in the brain and other neural tissues, raising concerns about its effect on the nervous system due to its prolonged biological half-life. Cd can enter into the neurons, hence increasing the production of Reactive Oxygen Species (ROS) in them and impairing their antioxidant defenses. Cd disrupts the Calcium (Ca2+) balance in neurons, affects the function of the mitochondria, and triggers cell death pathways. As a result of these pathways, the path to the development of many neurological diseases affected by environmental factors, especially Cd, such as Alzheimer\'s Disease (AD) and Amyotrophic Lateral Sclerosis (ALS) is facilitated. There are cognitive deficits associated with long exposure to Cd. Memory disorders are present in both animals and humans. Cd alters the brain\'s function and performance in critical periods. There are lifelong consequences of Cd exposure during critical brain development stages. The susceptibility to neurotoxic effects is increased by interactions with a variety of risk factors. Cd poses risks to neuronal function and behavior, potentially contributing to neurodegenerative diseases like Parkinson\'s disease (PD) and AD as well as cognitive issues. This article offers a comprehensive overview of Cd-induced neurotoxicity, encompassing risk assessment, adverse effect levels, and illuminating intricate pathways.

Neuroinflammation is a process involved in a variety of central nervous system (CNS) diseases and is being increasingly recognized as a key mediator of cognitive impairments. Neuroinflammatory responses including glial activation, increased production of proinflammatory cytokines, and aberrant neuronal signaling, contribute to cognitive dysfunctions. Histamine is a key peripheral inflammatory mediator, but plays an important role in neuroinflammatory processes as well. The unique localization of histamine H3 receptor (H3R) in the CNS along with the modulation of the release of other neurotransmitters via its action on heteroreceptors on non-histaminergic neurons have led to the development of several H3R ligands for various brain diseases. H3R antagonists/ inverse agonists have revealed potential to treat diverse neuroinflammatory CNS disorders, including neurodegenerative diseases, attention-deficit hyperactivity syndrome and schizophrenia. In this mini review, we provide a brief overview on the crucial involvement of the histaminergic transmission in the neuroinflammatory processes underlying these cognitive disorders, with a special focus on H3R involvement. The anti-neuroinflammatory potential of single-targeted and multi-targeted H3R antagonists/inverse agonists for the treatment of these conditions is discussed here.

Knowledge of performance in activities of daily living and quality of life is important for management decisions and research endpoints. The use of harmonized scales is essential for objective assessment of both caregivers and patients with dementia with Lewy bodies. Functionality and quality of life are more impaired in dementia with Lewy bodies than in Alzheimer\'s disease, mostly due to higher prevalence of behavioral symptoms and motor manifestations in dementia with Lewy bodies. More longitudinal studies are required to assess if causality mediates the associations of clinical features with functional independence and worsened quality of life in these patients.

Wernicke\'s encephalopathy (WE) is a rare, life-threatening condition in which thiamine deficiency causes dysfunction of the Kreb\'s cycle, accumulation of lactic acid in the brain tissues, and irreversible cognitive impairment. Prompt treatment with IV thiamine can reverse the process. The classic Wernicke\'s triad of ataxia, memory issues, and ocular abnormalities is not often present. Caine\'s criteria, which requires two of the following: dietary deficiencies, ocular abnormalities, altered cognition or mental status, and cerebellar dysfunction, is highly sensitive and specific for Wernicke\'s diagnosis, especially in patients with alcohol use disorder. Refeeding syndrome (RS) has similar risk factors to WE, including disease states that lead to malnutrition. Patients with RS develop WE due to thiamine depletion that occurs when oral nutrition is reinitiated after a period of poor oral intake. We present a patient with initially undetected WE who developed RS after the initiation of treatment with IV thiamine. RS prolonged the neurologic symptoms of WE and led to an extended hospital stay and significant physical debility. In our patient, WE preceded RS instead of occurring as a consequence of it. The case highlights that if one of these disorders is present, the other may not be far behind. When WE precedes RS, prolonged treatment with IV thiamine may be warranted until the symptoms of both disorders resolve.

UNASSIGNED: Cognitive impairment is a common nonmotor symptom in Parkinson\'s disease (PD). Individuals of Latino background are traditionally underrepresented in research on PD. Despite the fact that Latinos comprise 18% of the U.S. population, they commonly make up less than 5% of samples in studies of PD. Emerging evidence suggests that Latino individuals with PD may experience disparities relative to White non-Latinos in terms of having more severe motor symptoms, more severe depressive symptoms, and worse health-related quality of life. The purpose of the present study was to investigate differences in cognitive performance between Latino and White non-Latino individuals with PD and examine correlates of cognitive performance.
UNASSIGNED: Data were obtained from the Parkinson\'s Progression Markers Initiative. Participants included 60 Latino individuals with PD and 1,009 White non-Latino individuals with PD, all of whom were followed annually for up to 5 years. Participants completed neuropsychological tests of attention and working memory, processing speed, visuospatial functioning, verbal fluency, and immediate and delayed memory and recall.
UNASSIGNED: Relative to White non-Latino individuals with PD, Latino individuals with PD had significantly lower scores on the global measure of cognitive functioning, a test of processing speed, and tests of working memory and attention. Years of education was the strongest correlate of performance in these three cognitive domains among individuals in the Latino group.
UNASSIGNED: These findings provide initial evidence of disparities in cognitive functioning among Latino individuals with PD. Educational disadvantages may be one potential driver of these disparities.

UNASSIGNED: Neurofibromatosis type 1 (NF type 1) is an autosomal dominant disease with typical clinical manifestations, such as skin lesions, Lisch nodules, optic pathway gliomas, and neurofibromas, caused by the mutation of the NF1 gene. Visual evoked potentials (VEP) present a measure of the electrophysiological response of visual cortex to a visual stimulus. The role of VEP in the pathophysiology of NF type 1 is very complex and requires additional research.
UNASSIGNED: We examined the differences between NF type 1 patients with normal and altered VEP and analyzed the correlation between the prolongation of P100 latency and disease severity.
UNASSIGNED: Two groups were formed: a control group and a study group with NF type 1 patients. Based on the control group analysis, a threshold value for a normal VEP finding of 116 ms was obtained, and it was used to divide the study group into subgroups with normal and altered VEP. We proceeded with examining the differences in clinical manifestations of the disease between the subgroups, after which we checked if there is a correlation between the prolongation of the P100 latency and the severity of the clinical picture according to the Riccardi scale. Statistical analysis was performed using the Pearson chi-square test and the Spearman correlation test in the program SPSS 28.0, with levels of statistical significance p = 0.05 and p = 0.001.
UNASSIGNED: In the group with the abnormal VEP we found a statistically significant more frequent occurrence of optic tract glioma (p = 0.008), tumors (p = 0.032), epilepsy (p = 0.043), and cognitive disorders (p = 0.028), while the other clinical signs had an equal prevalence in both groups. A moderately strong correlation (r s = 0.665) was observed between the prolongation of P100 latency and the severity of the clinical picture.
UNASSIGNED: Our results showed the important role of VEP in the description of clinical phenotypes of NF type 1. The authors of the study propose VEP to be included in the diagnostic algorithms designed for patients with NF type 1.

Postoperative cognitive dysfunction (POCD) is a major concern, particularly among older adults. This study used social isolation (ISO) and multiomics analyses in aged mice to investigate potential mechanisms underlying POCD development. Aged mice were divided into two groups: ISO and paired housing (PH). Oleamide and the cannabinoid receptor type 2 (CB2R) antagonist AM630 were administered intraperitoneally, while Foxq1 adeno-associated viral (AAV) vector was injected directly into the hippocampus. Intramedullary tibial surgeries were subsequently performed to establish the POCD models. Behavioral tests comprising the Y-maze, open field test, and novel object recognition were conducted 2 days after surgery. Hippocampal and serum inflammatory cytokines were assessed. Following surgery, ISO mice demonstrated intensified cognitive impairments and escalated inflammatory markers. Integrative transcriptomic and metabolomic analysis revealed elevated oleamide concentrations in the hippocampus and serum of PH mice, with associative investigations indicating a close relationship between the Foxq1 gene and oleamide levels. While oleamide administration and Foxq1 gene overexpression substantially ameliorated postoperative cognitive performance and systemic inflammation in mice, CB2R antagonist AM630 impeded these enhancements. The Foxq1 gene and oleamide may be crucial in alleviating POCD. While potentially acting through CB2R-mediated pathways, these factors may modulate neuroinflammation and attenuate proinflammatory cytokine levels within the hippocampus, substantially improving cognitive performance postsurgery. This study lays the groundwork for future research into therapeutic approaches targeting the Foxq1-oleamide-CB2R axis, with the ultimate goal of preventing or mitigating POCD.

UNASSIGNED: There is a trend toward fostering well-being, or the state of being happy and healthy, within the medical community. Historically, resident physicians have faced high rates of distress during training. A structured well-being curriculum in residency programs may shift residents\' mindsets from survival and resilience to one centered on purpose, engagement, and joy.
UNASSIGNED: An original well-being curriculum was administered to residents in person at a single institution every 5 weeks for approximately 10 well-being workshops, totaling around 20 hours of curriculum exposure during every academic year. The well-being curriculum was divided into 4 domains: cognitive distortions and problematic mindsets, mindfulness and meditation, creative outlets, and self-compassion.Residents exposed to at least 1 year of the well-being curriculum were asked to answer an anonymous survey. Four questions were asked for each of the 4 domains. The first and second questions asked how familiar they were with the topic before and after the workshops on a scale of 1-5 of familiarity. The third and fourth questions asked how much the knowledge acquired influenced their professional and personal life on a scale of 1-5 of influence.
UNASSIGNED: Before curriculum exposure, the average for moderate or higher levels of knowledge across all domains was 22.7%, which improved to 77.3% after curriculum completion. Overall, 58.6% of participants felt the knowledge of the domains was moderately or extremely influential in their professional lives and 83.6% in their personal lives. There were no significant differences between post-graduate year 2 and post-graduate year 3 residents for any domains examined before and after the wellness workshops.
UNASSIGNED: A 4-domain well-being curriculum practiced in a group setting positively impacted participating residents in their personal and professional lives. Further studies need to be performed on a larger scale to assess if the curriculum fits the needs of the broader medical community.