The dentate nucleus was examined histologically and immunohistochemically in 47 cases of nonprogressive developmental disorders. Neuronal loss and/or atrophy was observed in 13 cases, while mild neuronal lesions, characterized by dendritic swelling and/or the appearance of eosinophilic materials around the neurons, were exhibited in 20 cases. The former change was accompanied by diffuse central nervous system involvement, and the etiology was perinatal hypoxic ischemic encephalopathy, acute encephalopathy, and meningoencephalitis in most cases. On the other hand, most of the patients with kernicterus showed the latter change. Immunohistochemically, the mild neuronal lesions mimicking grumose, degeneration, described in some neurodegenerative diseases, seemed to reflect the changes of Purkinje cell terminals. It is suggested that secondary structural alteration of the dentate neurons in the absence of severe atrophy can occur in nonprogressive developmental disorders.
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iScience
January 2025
Cognitive Neuroimaging Unit U992, CNRS, INSERM, CEA, DRF/Institut Joliot, Université Paris-Saclay, NeuroSpin Center, 91191 Gif/Yvette, France.
The need for attention to enable statistical learning is debated. Testing individuals with impaired consciousness offers valuable insight, but very few studies have been conducted due to the difficulties inherent in such studies. Here, we examined the ability of patients with varying levels of disorders of consciousness (DOC) to extract statistical regularities from an artificial language composed of randomly concatenated pseudowords by measuring frequency tagging in EEG.
View Article and Find Full Text PDFFront Neurosci
January 2025
Department of Experimental Pharmacology, Mossakowski Medical Research Institute, Polish Academy of Sciences, Warsaw, Poland.
Over the last three decades, dynamically evolving research using novel technologies, including virtual environments (VEs), has presented promising solutions for neuroscience and neuropsychology. This article explores the known and potential benefits and drawbacks of employing modern technologies for diagnosing and treating developmental disorders, exemplified by autism spectrum disorder (ASD). ASD's complex nature is ideal for illustrating the advantages and disadvantages of the digital world.
View Article and Find Full Text PDFNat Commun
January 2025
College of Pharmaceutical Sciences, National Key Laboratory of Advanced Drug Delivery and Release Systems, Zhejiang University, Hangzhou, China.
Nicotinamide (NAM), a main precursor of NAD+, is essential for cellular fuel respiration, energy production, and other cellular processes. Transporters for other precursors of NAD+ such as nicotinic acid and nicotinamide mononucleotide (NMN) have been identified, but the cellular transporter of nicotinamide has not been elucidated. Here, we demonstrate that equilibrative nucleoside transporter 1 and 2 (ENT1 and 2, encoded by SLC29A1 and 2) drive cellular nicotinamide uptake and establish nicotinamide metabolism homeostasis.
View Article and Find Full Text PDFNeurobiol Dis
January 2025
Department of Neurology and Center for Neurodegeneration and Experimental Therapeutics, University of Alabama at Birmingham, Birmingham, AL 35294, USA; Southern Research, Birmingham, AL 35205, USA. Electronic address:
Mitochondrial dysfunction, transcriptional dysregulation, and protein aggregation are hallmarks of multiple neurodegenerative disorders, including Huntington's disease (HD). Strategies are needed to counteract these processes to restore neuronal health and function in HD. Recent evidence indicates that the transcription factor estrogen-related receptor gamma (ERRγ/Esrrg) is required for normal expression of mitochondrial, synaptic, and autophagy genes in neurons.
View Article and Find Full Text PDFBiol Psychiatry Cogn Neurosci Neuroimaging
January 2025
Department of Psychiatry, Washington University in St. Louis, School of Medicine, Saint Louis, MO, USA.
Background: The understanding of the neural correlates of borderline personality disorder (BPD) is limited, but suggests alterations in limbic structures play a role in adult BPD. The developmental course of structural neural differences in BPD is unknown. Whether there is specificity for structural alterations in BPD compared with other psychiatric presentations, such as major depressive disorder (MDD), remains unexplored.
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