Atrophic brain changes in acute anorexia nervosa (AN) are often visible to the naked eye on computed tomography or magnetic resonance imaging scans, but it remains unclear what is driving these effects. In neurological diseases, neurofilament light (NF-L) and tau protein have been linked to axonal damage. Glial fibrillary acidic protein (GFAP) has been associated with astroglial injury. In an attempt to shed new light on factors potentially underlying past findings of structural brain alterations in AN, the current study investigated serum NF-L, tau protein, and GFAP levels longitudinally in AN patients undergoing weight restoration. Blood samples were obtained from 54 acutely underweight, predominantly adolescent female AN patients and 54 age-matched healthy control participants. AN patients were studied in the severely underweight state and again after short-term partial weight restoration. Group comparisons revealed higher levels of NF-L, tau protein, and GFAP in acutely underweight patients with AN compared to healthy control participants. Longitudinally, a decrease in NF-L and GFAP but not in tau protein levels was observed in AN patients upon short-term partial weight restoration. These results may be indicative of ongoing neuronal and astroglial injury during the underweight phase of AN. Normalization of NF-L and GFAP but not tau protein levels may indicate an only partial restoration of neuronal and astroglial integrity upon weight gain after initial AN-associated cell damage processes.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC7870648 | PMC |
http://dx.doi.org/10.1038/s41398-021-01209-w | DOI Listing |
Ecotoxicol Environ Saf
January 2025
Department of Occupational Medicine and Environmental Toxicology, Nantong Key Laboratory of Environmental Toxicology, School of Public Health, Nantong University, Nantong 226019, China. Electronic address:
Nanoplastics are common environmental pollutants. As of now, research has yet to explore how exposure to nanomaterials during gestation might influence the risk of developing Alzheimer's disease (AD) in offspring. Throughout the research, we assessed the AD pathology in adult offspring of mice prenatal 80 nm polystyrene nanoparticles (PS-NPs) exposure.
View Article and Find Full Text PDFBiomed Pharmacother
January 2025
Institut de Neurociències (INc), Universitat Autònoma Barcelona, Bellaterra 08193, Spain; Vall d'Hebron Institut de Recerca (VHIR), Barcelona 08035, Spain; Institució Catalana de Recerca i Estudis Avançats (ICREA), Barcelona 08010, Spain. Electronic address:
Alzheimer's disease (AD) is a prevalent neurodegenerative disorder characterized by amyloid-β and Tau protein depositions, with treatments focusing on single proteins have shown limited success due to the complexity of pathways involved. This study explored the potential of chronokines -proteins that modulate aging-related processes- as an alternative therapeutic approach. Specifically, we focused on a novel pleiotropic chimeric protein named HEBE, combining s-KL, sTREM2 and TIMP2, guided by bioinformatic analyses to ensure the preservation of each protein's conformation, crucial for their functions.
View Article and Find Full Text PDFIntroduction: Age-associated depletion in nicotinamide adenine dinucleotide (NAD+) concentrations has been implicated in metabolic, cardiovascular, and neurodegenerative disorders. Supplementation with NAD+ precursors, such as nicotinamide riboside (NR), offers a potential therapeutic avenue against neurodegenerative pathologies in aging, Alzheimer's disease, and related dementias. A crossover, double-blind, randomized placebo (PBO) controlled trial was conducted to test the safety and efficacy of 8 weeks' active treatment with NR (1 g/day) on cognition and plasma AD biomarkers in older adults with subjective cognitive decline and mild cognitive impairment.
View Article and Find Full Text PDFTransl Androl Urol
December 2024
Department of Urology, Xinjiang Medical University Affiliated Tumor Hospital, Urumqi, China.
Background: Speckle-type POZ protein (SPOP), FAS-associated protein with death domain (FADD), and nuclear transcription factor-κB (NF-κB) have been shown to be associated with the development of prostate cancer (PCa). FADD has been shown to activate the NF-κB pathway to promote tumorigenesis, while SPOP has been shown to enhance the breakdown of FADD and inhibit the function of the NF-κB signaling pathway in non-small cell lung cancer. The existence of this mechanism has not yet been confirmed in PCa.
View Article and Find Full Text PDFTransl Androl Urol
December 2024
Department of Urology, The Second Affiliated Hospital of Chongqing Medical University, Chongqing, China.
Background: Some studies suggest a potential association between plasma lipidome and erectile dysfunction (ED), but the underlying mechanism and whether circulating inflammatory proteins act as mediators remain unclear. The purpose of this study was to investigate the potential causal relationships between plasma lipidome, inflammatory proteins, and ED.
Methods: Plasma lipidome, circulating inflammatory proteins, and ED cases were identified based on the summary data from several large-scale genome-wide association studies (GWAS).
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!