Category Ranking
98%
Total Visits
921
Avg Visit Duration
2 minutes
Citations
20
Article Abstract
Background: Patients with bipolar disorder (BD) are highly at risk for dementia and may develop brain atrophy, which is linked to cognitive decline. One possible reason for brain atrophy is cellular damage resulting from waste product accumulation caused by glymphatic dysfunction. This study evaluated the glymphatic system in patients with BD, using diffusion tensor image analysis along the perivascular space (DTI-ALPS) and choroid plexus volume (CPV) in two separate BD cohorts. The insight into whether these clearance indices were associated with brain atrophy was also investigated.
Methods: The discovery cohort consisted of 28 patients with BD and 28 healthy controls (HCs). The validation cohort included 42 patients with BD and 42 HCs. BD group and HCs in both cohorts underwent group comparisons of the ALPS index, CPV relative to the total intracranial volume (CPV/TIV), and brain gray matter volume. The relationships between the ALPS index and frontal pole volume were determined.
Results: The ALPS index decreased in BD group compared with that in HCs in both cohorts (p < 0.05). While BD group showed increased CPV/TIV and frontal pole atrophy in the discovery cohort, such increase was insignificant in the validation cohort. In the discovery cohort, frontal pole atrophy was related to the ALPS index decrement (r = 0.34, p = 0.02), and the ALPS index-mediated frontal pole atrophy was associated with BD.
Conclusion: Middle-aged patients with BD may experience dysfunction in the excretory pathway of the perivascular space around the medullary veins, likely contributing to frontal pole atrophy.
Download full-text PDF |
Source |
|---|---|
| http://dx.doi.org/10.1016/j.jad.2025.119686 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
Cortical Thinning and Microstructural Integrity Disruption in White Matter Hyperintensities.
Brain Res Bull
September 2025
Department of Neurology, The Second Affiliated Hospital of Anhui Medical University, 230601, He Fei, China; Collaborative Innovation Center of Neuropsychiatric Disorders and Mental Health, 230032, Hefei, China; Anhui Province Key Laboratory of Cognition and Neuropsychiatric Disorders, 230032, Hefei,
Background: The relationships between white matter microstructure, cortical atrophy, and cognitive function in cerebral small vessel disease (CSVD)-related white matter hyperintensities (WMHs) patients are unclear.
Methods: 71 right-handed WMHs patients (mild, n=23; moderate, n=27; severe, n=21) and 35 healthy controls were included. Tract-based spatial statistics (TBSS) assessed microstructure via fractional anisotropy (FA) and mean diffusivity (MD).
Relation of Visual Function, Retinal Thickness by Optical Coherence Tomography, and MRI Brain Volume in Pediatric-Onset Multiple Sclerosis.
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.
Alterations of the brain functional organization in young-onset Alzheimer's disease: Is it a matter of "time"?
J Alzheimers Dis
September 2025
Frontotemporal Disorders Unit, Department of Neurology, Massachusetts General Hospital and Harvard Medical School, Charlestown, MA, USA.
Compared with more typical late-onset Alzheimer's disease (AD), the mechanisms of young-onset AD (YOAD; age of symptom onset <65 years) remain less understood. Using resting-state functional MRI data and dynamic causal modeling techniques, Sacu et al. demonstrate that individuals with YOAD (amnestic AD or posterior cortical atrophy) exhibit alterations in effective (i.
View Article and Find Full Text PDFPrenatal SMN-dependent defects in translation uncover reversible primary cilia phenotypes in spinal muscular atrophy.
JCI Insight
September 2025
Edinburgh Medical School: Biomedical Sciences & Euan MacDonald Centre for M, University of Edinburgh, Edinburgh, United Kingdom.
Spinal muscular atrophy (SMA) is a neuromuscular disease caused by low levels of SMN protein. Several therapeutic approaches boosting SMN are approved for human patients, delivering remarkable improvements in lifespan and symptoms. However, emerging phenotypes, including neurodevelopmental comorbidities, are being reported in some treated SMA patients, indicative of alterations in brain development.
View Article and Find Full Text PDFAbnormal Amyloid-β Duration, Tau, and Neurodegeneration in Cranial Images.
JAMA Netw Open
September 2025
School of Medicine and Public Health, University of Wisconsin-Madison, Madison.
Importance: It is unclear whether the duration of amyloid-β (Aβ) pathology is associated with neurodegeneration and whether this depends on the presence of tau.
Objective: To examine the association of longitudinal atrophy with Aβ positron emission tomography (PET)-positivity (Aβ+) and the estimated duration of Aβ+ (Aβ+ duration), controlling for tau-positivity.
Design, Setting, And Participants: Data for this longitudinal cohort study were drawn from the Wisconsin Registry for Alzheimer Prevention and the Wisconsin Alzheimer Disease Research Center Clinical Core Study.