The purpose of the present study is to try an alternative way of analyzing the ABR (Auditory Brainstem Response). The stimuli were complex sounds (c-ABR) as used in earlier studies. It was further aimed at corroborating earlier findings that this method can discriminate several neuropsychiatric states. Forty healthy control subjects, 26 subjects with the diagnosis schizophrenia (Sz) and 33 with ADHD (Attention deficit hyperactivity disorder) were recruited for the study. The ABRs were recorded. The analysis was based on calculation of areas of significantly group different time spans in the waves. Both latency and amplitude were thereby influential. The spans of differences were quantified for each subject in relation to the total area of the curve which made comparisons balanced. The results showed highly significant differences between the study groups. The results are important for future work on identifying markers for neuropsychiatric clinical use. To reach that goal calls for more extensive studies than this preliminary one.
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http://dx.doi.org/10.1016/j.neulet.2016.08.041 | DOI Listing |
PLoS One
January 2025
Neuroscience Discovery, Janssen Research & Development, Janssen Pharmaceutica, Beerse, Belgium.
The MAPT gene encodes Tau protein, a member of the large family of microtubule-associated proteins. Tau forms large insoluble aggregates that are toxic to neurons in several neurological disorders, and neurofibrillary Tau tangles represent a key pathological hallmark of Alzheimer's disease (AD) and other tauopathies. Lowering Tau expression levels constitutes a potential treatment for AD but the mechanisms that regulate Tau expression at the transcriptional or translational level are not well understood.
View Article and Find Full Text PDFTissue Eng Part B Rev
January 2025
Research Unit in Mineralized Tissue Reconstruction and Faculty of Dentistry, Thammasat University, Pathum Thani, Thailand.
The increasing number of elderly people across the globe has led to a rise in osteoporosis and bone fractures, significantly impacting the quality of life and posing substantial health and economic burdens. Despite the development of tissue-engineered bone constructs and stem cell-based therapies to address these challenges, their efficacy is compromised by inadequate vascularization and innervation during bone repair. Innervation plays a pivotal role in tissue regeneration, including bone repair, and various techniques have been developed to fabricate innervated bone scaffolds for clinical use.
View Article and Find Full Text PDFMol Neurobiol
January 2025
Department of Pathology and Applied Neurobiology, Kyoto Prefectural University of Medicine, Graduate School of Medical Science, 465 Kajii-Cho, Kawaramachi Hirokoji, Kamigyo-Ku, Kyoto, 602-8566, Japan.
Duchenne/Becker muscular dystrophy (DMD/BMD) manifests progressive muscular dystrophy and non-progressive central nervous disorder. The neural disorder is possibly caused by abnormalities in the developmental period; however, basic research to understand the mechanisms remains underdeveloped. The responsible gene, Dmd (dystrophin), generates multiple products derived from several gene promoters.
View Article and Find Full Text PDFGlia
January 2025
Key Laboratory of Organ Regeneration and Reconstruction, Institute of Zoology, Chinese Academy of Sciences, Beijing, China.
Traumatic brain injury (TBI) is a leading cause of death and disability worldwide, with limited effective treatment strategies. Endogenous neural stem cells (NSCs) give rise to neurons and glial cells throughout life. However, NSCs are more likely to differentiate into glial cells rather than neurons at the lesion site after TBI and the underlying molecular mechanism remains largely unknown.
View Article and Find Full Text PDFGlia
January 2025
Department of Neurology, University of Washington School of Medicine, Seattle, Washington, USA.
Human genetics studies lent firm evidence that microglia are key to Alzheimer's disease (AD) pathogenesis over a decade ago following the identification of AD-associated genes that are expressed in a microglia-specific manner. However, while alterations in microglial morphology and gene expression are observed in human postmortem brain tissue, the mechanisms by which microglia drive and contribute to AD pathology remain ill-defined. Numerous mouse models have been developed to facilitate the disambiguation of the biological mechanisms underlying AD, incorporating amyloidosis, phosphorylated tau, or both.
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