This study explores the complex link between vitamin D and neurological illnesses, focusing on how vitamin D affects possible risk factors, therapeutic applications, and the trajectory of the disease. An epidemiological study has linked vitamin D insufficiency to several neurological conditions, including Parkinson's disease, Alzheimer's disease, and multiple sclerosis. It is hypothesized that immunomodulatory and anti-inflammatory properties of vitamin D contribute to its neuroprotective effects. Two major mechanisms in dementia include neuroinflammation and oxidative stress. Adequate levels of vitamin D have been shown in both animal models and human studies to enhance both clinical outcomes and the duration of illness in those who have it. Other ways that vitamin D contributes to its therapeutic potential include the production of neurotrophic factors, control over neurotransmitter synthesis, and preservation of the blood-brain barrier. Despite the encouraging outcomes, research is still being conducted to determine the optimal dosage and long-term benefits of vitamin D supplementation on brain function. In order to furnish precise directives and clarify the processes behind the neuroprotective impacts of vitamin D, future research must focus on large-scale randomized controlled studies. . This study highlights the significance of maintaining adequate levels of vitamin D as a modifiable risk factor for neurological disorders. Further study is also required to comprehend the possible medical benefits of this vitamin fully.
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http://dx.doi.org/10.2174/0118715273330972241009092828 | DOI Listing |
Int J Colorectal Dis
January 2025
Internal Medicine, Jilin Cancer Hospital, Changchun, China.
Purpose: This phase II study is designed to evaluate the combination therapy involving suvemcitug and envafolimab with FOLFIRI in microsatellite-stable or mismatch repair-proficient (MSS/pMMR) colorectal cancer (CRC) in the second-line treatment setting.
Methods: This study is a non-randomized, open-label prospective study comprising multiple cohorts (NCT05148195). Here, we only report the data from the CRC cohort.
J Pediatr Gastroenterol Nutr
January 2025
Division of Pediatric Gastroenterology, Louisiana State University-Health Science Center, New Orleans, Louisiana, USA.
Objectives: Inflammatory bowel disease (IBD) results from genetic susceptibility, gut microbiome, and environmental factors. Diet, one modifiable environmental factor, has been linked to the increased prevalence of IBD. This study aimed to evaluate a potential association between food deserts and disease severity at diagnosis.
View Article and Find Full Text PDFInt J Rheum Dis
January 2025
Department of Rheumatology, Ankara Bilkent City Hospital, Ankara, Türkiye.
Objective: To investigate the central sensitization (CS) in patients with autoimmune connective tissue diseases (ACTDs) and its relationship with disease activity, laboratory findings, medical treatments, organ involvements, and comorbidity.
Methods: One hundred and eleven patients with ACTDs and 40 healthy individuals were included. All patients were divided into three groups in terms of their diseases: Sjögren's syndrome (SS), rheumatoid arthritis (RA), and systemic lupus erythematosus (SLE).
Front Public Health
January 2025
Department of Statistics, Bahir Dar University, Bahir Dar, Ethiopia.
Introduction: Childhood vaccinations are crucial in safeguarding children from infectious diseases and are recognized as one of the most cost-effective public health interventions. However, children in East African countries face more than a fifteen-fold increased risk of death from vaccine-preventable diseases compared to those in high-income nations. This study aimed to identify the factors influencing childhood immunization status in East Africa.
View Article and Find Full Text PDFFront Aging
January 2025
Cellular and Molecular Neurobiology & Drug Targeting Laboratory, Department of Zoology, Indira Gandhi National Tribal University, Amarkantak, Madhya Pradesh, India.
Memory formation is associated with constant modifications of neuronal networks and synaptic plasticity gene expression in response to different environmental stimuli and experiences. Dysregulation of synaptic plasticity gene expression affects memory during aging and neurodegenerative diseases. Covalent modifications such as methylation on DNA and acetylation on histones regulate the transcription of synaptic plasticity genes.
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