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| http://dx.doi.org/10.1136/bcr-2013-201695 | DOI Listing |
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Abnormalities in rich-club connections are associated with an exacerbation of genetic susceptibility to schizophrenia.
BMC Psychiatry
December 2024
The Affiliated People's Hospital of Jiangsu University, Zhenjiang First People's Hospital, No.8, Dianli Road, Zhenjiang, 212002, Jiangsu, China.
Background: Schizophrenia (SZ) is a highly heritable and heterogeneous disorder that is often associated with widespread structural brain abnormalities. However, the causes of interindividual differences in genetic susceptibility remain largely unknown. This study attempted to address this important issue by utilizing a prospective study in which unaffected first-degree relatives of SZ (FH+) were recruited.
View Article and Find Full Text PDFGender differences of neurometabolic and neuroendocrine alternations and its lateralization in adolescents with major depressive disorder.
BMC Psychiatry
December 2024
Department of Psychiatry, First Affiliated Hospital, Jinan University, Guangzhou, 510630, China.
Background: The clinical characteristics of major depressive disorder (MDD) in adolescents show notable gender-related differences, but the cause of these differences is still not understood. The current research concentrates on the changes in neurometabolism and neuroendocrine function, aiming to identify differences in endocrine function and brain metabolism between male and female adolescents with MDD.
Methods: A total of 121 teenagers diagnosed with MDD (43 males and 78 females) were enlisted as participants.
Updated imaging markers in cerebral amyloid angiopathy: What radiologists need to know.
Jpn J Radiol
December 2024
Department of Radiology, Mie University Graduate School of Medicine, 2-174, Edobashi, Tsu, Mie, 514-8507, Japan.
Cerebral amyloid angiopathy (CAA) is an age-related small vessel disease pathologically characterized by the progressive accumulation of amyloid-beta (Aβ) peptide in cerebrovascular walls, affecting both cortical and leptomeningeal vessels. Amyloid deposition results in fragile vessels, which may lead to lobar intracerebral hemorrhage (ICH) and cognitive impairment. To evaluate the probability and severity of CAA, the imaging markers depicted on CT and MRI techniques are crucial, as brain pathological examination is highly invasive.
View Article and Find Full Text PDFGenetic risk for treatment resistant schizophrenia and corresponding variation in dopamine synthesis capacity and D receptor availability in healthy individuals.
Mol Psychiatry
December 2024
From the Clinical & Translational Neuroscience Branch, Intramural Research Program, National Institute of Mental Health, NIH, DHHS, Bethesda, MD, 20892, USA.
Dysfunction of dopamine systems has long been considered a hallmark of schizophrenia, and nearly all current first-line medication treatments block dopamine D receptors. However, approximately a quarter of patients will not adequately respond to these agents and are considered treatment-resistant. Whereas abnormally high striatal presynaptic dopamine synthesis capacity has been observed in people with schizophrenia, studies of treatment-resistant patients have not shown this pattern and have even found the opposite - i.
View Article and Find Full Text PDFNuclear respiratory factor-1 (NRF1) induction drives mitochondrial biogenesis and attenuates amyloid beta-induced mitochondrial dysfunction and neurotoxicity.
Neurotherapeutics
December 2024
Department of Nanomedicine, Houston Methodist Research Institute, Houston, TX, 77030, USA; Department of Medicine, Weill Cornell Medical College, New York, NY, 10065, USA; Department of Cardiology, Houston Methodist DeBakey Heart and Vascular Center, Houston Methodist Hospital, Houston, TX, 77030, USA. Electronic address:
Mitochondrial dysfunction is an important driver of neurodegeneration and synaptic abnormalities in Alzheimer's disease (AD). Amyloid beta (Aβ) in mitochondria leads to increased reactive oxygen species (ROS) production, resulting in a vicious cycle of oxidative stress in coordination with a defective electron transport chain (ETC), decreasing ATP production. AD neurons exhibit impaired mitochondrial dynamics, evidenced by fusion and fission imbalances, increased fragmentation, and deficient mitochondrial biogenesis, contributing to fewer mitochondria in brains of AD patients.
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