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Background: Extensive neuroimaging studies have established that functional abnormalities and morphological alterations in the nucleus accumbens (NAc) are implicated in major depressive disorder (MDD), but changes in its white matter structural connectivity (SC) remain unclear. We aimed to elucidate the changes in the white matter fibre connectivity of the NAc in MDD patients.
Methods: This study used probabilistic fibre tracking to analyze the diffusion tensor imaging (DTI) data of 125 MDD patients and 129 healthy controls (HCs), calculating the strength of SC (sSC) from bilateral NAc to the entire brain and its correlation with depressive symptoms.
Results: Compared to HCs, MDD exhibited increased sSC between the left NAc (L.NAc) and regions involving the left middle frontal gyrus, bilateral cingulate gyrus (CG), bilateral hippocampus, left caudate, left medial superior occipital gyrus, right globus pallidus, right superior and middle temporal gyrus, right precuneus, right insula, and right posterior parietal thalamus. Enhanced sSC was also observed between the right NAc (R.NAc) and the left temporal lobe, left posterior superior temporal sulcus (pSTS), bilateral lateral occipital cortex, left hippocampus, right putamen and right ventral occipital cortex. The sSC of L.NAc-left CG and R.NAc-left pSTS was positively correlated with HAMD scores in MDD.
Conclusions: Abnormal white matter connectivity of the NAc primarily affects the cortico-limbic circuit, cortico-basal ganglia circuit, and the temporal-occipital cortical regions in patients with MDD, along with the asymmetrical features of the inter-hemispheric SC related to NAc. These alteration may underlie the dysfunction of reward processing and emotion regulation in MDD.
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http://dx.doi.org/10.1016/j.jad.2025.03.182 | DOI Listing |
Neurology
October 2025
Norcliffe Foundation Center for Integrative Brain Research, Seattle Children's Research Institute, WA.
Background And Objectives: Neuroimaging findings in immune effector cell-associated neurotoxicity syndrome (ICANS) have not been systematically described. We created the chimeric antigen receptor (CAR) T-cell Neurotoxicity Imaging Virtual Archive Library (CARNIVAL), a centralized imaging database for children and young adults receiving CAR T-cell therapy. Objectives of this study were to (1) characterize neuroimaging findings associated with ICANS and (2) determine whether specific ICANS-related neuroimaging findings are associated with individual neurologic symptoms.
View Article and Find Full Text PDFTrop Doct
September 2025
Additional Professor, Department of Radiodiagnosis, Postgraduate Institute of Medical Education and Research, Chandigarh, India.
Chikungunya virus (CHIKV) typically causes febrile illness and arthralgia. However, severe complications such as encephalitis, rhabdomyolysis, and multiorgan dysfunction are increasingly recognised, particularly during epidemics in endemic regions. We report a case of a 61-year old male presenting with progressive flaccid paraparesis and respiratory failure following febrile illness.
View Article and Find Full Text PDFNeurochem Res
September 2025
International Translational Neuroscience Research Institute, Zhejiang Chinese Medical University, Hangzhou, 310053, Zhejiang, China.
The concept of the central nervous system (CNS) reserve emerged from the mismatch often observed between the extent of brain pathology and its clinical manifestations. The cognitive reserve reflects an "active" capacity, driven by the plasticity of CNS cellular components and shaped by experience, learning, and memory processes that increase resilience. We propose that neuroglial cells are central to defining this resilience and cognitive reserve.
View Article and Find Full Text PDFJ Cereb Blood Flow Metab
September 2025
iInstitut de Mécanique des Fluides de Toulouse (IMFT), Université de Toulouse, CNRS, INPT, Université Toulouse III - Paul Sabatier (UPS), Toulouse, France.
Cerebral Amyloid Angiopathy, a common age-related small vessel disease leading to hemorrhagic stroke, shares many characteristics with Alzheimer's disease: toxic amyloid deposits, microvascular alterations and enlarged perivascular spaces (EPVS). Together, PVS enlargement, reduced amyloid-β clearance and further accumulation form a vicious cycle underlying disease progression. Yet, the neuropathological correlates of EPVS, including the associated angioarchitecture, are poorly understood.
View Article and Find Full Text PDFJ Integr Neurosci
August 2025
Key Laboratory of Modern Toxicology of Ministry of Education; School of Basic Medical Sciences, Nanjing Medical University, 211166 Nanjing, Jiangsu, China.
Cognitive impairment represents a progressive neurodegenerative condition with severity ranging from mild cognitive impairment (MCI) to dementia and exerts significant burdens on both individuals and healthcare systems. Vascular cognitive impairment (VCI) represents a heterogeneous clinical continuum, spanning a spectrum from subcortical ischemic VCI (featuring small vessel disease, white matter lesions, and lacunar infarcts) to mixed dementia, where vascular and Alzheimer's-type pathologies coexist. While traditionally linked to macro- and microvascular dysfunction, the mechanisms underlying VCI remain complex.
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