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Background: Asthma is a common chronic respiratory disease, and its potential association with the central nervous system has garnered increasing attention in recent years. While observational studies suggest that asthma may affect hippocampal structure and function through mechanisms such as chronic inflammation and hypoxia, its causal relationship remains unclear.
Methods: In this study, we employed a two-sample Mendelian randomization (MR) analysis, utilizing large-scale genome-wide association study (GWAS) data to systematically investigate the potential causal relationship between asthma and hippocampal volume. Data from a GWAS of asthma involving 155,386 individuals of European ancestry and GWAS imaging-derived phenotypes (IDPs) of hippocampal volume from 33,219 European individuals were analyzed.
Results: The results revealed a significant negative correlation between asthma and multiple hippocampal IDPs (P < 0.05), indicating that asthma may contribute to reduced hippocampal volume. We identified 19 independent SNPs significantly associated with asthma (P < 5×10⁻⁸), of which 16 SNPs were retained after clumping (r < 0.001) and harmonization. Sensitivity analyses revealed no heterogeneity or horizontal pleiotropy, and reverse MR analysis did not support a causal effect of hippocampal volume on asthma.
Conclusion: Our study provides genetic evidence for a causal relationship between asthma and changes in hippocampal volume, highlighting the need for closer monitoring and intervention in the neurocognitive health of asthma patients in clinical practice. Future studies should explore the causal relationship between asthma and brain structural changes across different racial groups and asthma subtypes, as well as the underlying biological mechanisms.
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http://dx.doi.org/10.1002/brb3.70560 | DOI Listing |
Neuroimage Clin
September 2025
Department of Women's and Children's Health, Karolinska Institutet, Stockholm, Sweden; Department of Biomedical and Clinical Sciences, Linköping University, Linköping, Sweden.
Objectives: To examine associations between low cognitive-performance and regional-and network-level brain changes at ages 9-10 in very-preterm, moderately-preterm, and full-term children, and explore whether these alterations predict ASD/ADHD symptoms at age 12.
Methods: This longitudinal population-based study included 9-10-year-old U.S.
Neurol Neuroimmunol Neuroinflamm
November 2025
Departments of Neurology and Ophthalmology, NYU Grossman School of Medicine, NY; and.
Background And Objectives: While reductions in optical coherence tomography (OCT) pRNFL and ganglion cell-inner plexiform layer thicknesses have been shown to be associated with brain atrophy in adult-onset MS (AOMS) cohorts, the relationship between OCT and brain MRI measures is less established in pediatric-onset MS (POMS). Our aim was to examine the associations of OCT measures with volumetric MRI in a cohort of patients with POMS to determine whether OCT measures reflect CNS neurodegeneration in this patient population, as is seen in AOMS cohorts.
Methods: This was a cross-sectional study with retrospective ascertainment of patients with POMS evaluated at a single center with expertise in POMS and neuro-ophthalmology.
J Alzheimers Dis
September 2025
The Framingham Heart Study, Framingham, MA, USA.
BackgroundWomen have a higher risk of dementia than men. Reproductive factors may be implicated.ObjectiveDetermine the association between reproductive factors (earlier menarche, later menopause, longer reproductive lifespan (RLS), post-menopausal hormone replacement therapy [pmHRT] use, and serum estradiol/estrone) and neurocognitive and neuroimaging markers of brain aging and incident dementia in cognitively healthy women.
View Article and Find Full Text PDFBiol Psychiatry Glob Open Sci
November 2025
University of Basel, Department of Clinical Research (DKF), University Psychiatric Clinics, Translational Neurosciences, Basel, Switzerland.
Background: The hippocampus plays a critical role in psychosis, with reduced volume observed across the psychosis continuum. These structural changes are associated with cognitive deficits, symptom severity, and increased risk of psychosis progression. Elevated hippocampal perfusion and glutamate/GABA (gamma-aminobutyric acid) imbalance further suggest metabolic dysregulation as a key mechanism.
View Article and Find Full Text PDFFront Aging Neurosci
August 2025
Digital Health Research Division, Korea Institute of Oriental Medicine, Daejeon, Republic of Korea.
Introduction: The role of triglycerides in Alzheimer's disease dementia (ADD) progression remains unclear. This study aimed to investigate how triglyceride levels influence the relationship between amyloid-beta (Aβ) deposition, hippocampal atrophy, and cognitive decline in individuals with mild cognitive impairment (MCI) and early-stage ADD.
Methods: A total 188 older adults (170 with MCI, 18 with early ADD) from the Gwangju Alzheimer's Disease and Related cohort underwent amyloid PET and structural magnetic resonance imaging.