Brain-derived neurotrophic factor (BDNF) influences the differentiation, plasticity, and survival of central neurons and likewise, affects the development of the neuromuscular system. Besides its neuronal origin, BDNF is also a member of the myokine family. However, the role of skeletal muscle-derived BDNF in regulating neuromuscular physiology in vivo remains unclear. Using gain- and loss-of-function animal models, we show that muscle-specific ablation of BDNF shifts the proportion of muscle fibers from type IIB to IIX, concomitant with elevated slow muscle-type gene expression. Furthermore, BDNF deletion reduces motor end plate volume without affecting neuromuscular junction (NMJ) integrity. These morphological changes are associated with slow muscle function and a greater resistance to contraction-induced fatigue. Conversely, BDNF overexpression promotes a fast muscle-type gene program and elevates glycolytic fiber number. These findings indicate that BDNF is required for fiber-type specification and provide insights into its potential modulation as a therapeutic target in muscle diseases.
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http://dx.doi.org/10.1073/pnas.1900544116 | DOI Listing |
J Ethnopharmacol
January 2025
School of Basic Medical Sciences, Shanxi University of Chinese Medicine, Jinzhong, Shanxi, 030619; Shanxi Provincial Key Laboratory of TCM Encephalopathy; National International Joint Research Center for Molecular Traditional Chinese Medicine. Electronic address:
Ethnopharmacological Relevance: Dihuang Drink (DHD), formulated by Liu Hejian during the Yuan Dynasty, is listed as one of the first ancient classical prescriptions by the National Medical Products Administration of China. It is commonly used for the prevention and treatment of Alzheimer's disease (AD). This study further investigates the therapeutic effects and potential mechanisms of DHD in AD.
View Article and Find Full Text PDFArch Gerontol Geriatr
December 2024
Neurology Ward 1, The First Affiliated Hospital of Guangxi University of Chinese Medicine, Qingxiu District, Nanning, 530001, China. Electronic address:
Purpose: The incidence of vascular dementia (VaD), as one of the main types of dementia in old age, has been increasing year by year, and exploring its pathogenesis and seeking practical and effective treatment methods are undoubtedly the key to solving this problem. Phosphoglycerate translocase 5 (PGAM5), as a crossroads of multiple signaling pathways, can lead to mitochondrial fission, which in turn triggers the onset and development of necroptosis, and thus PGAM5 may be a novel target for the prevention and treatment of vascular dementia.
Methods: Animal model of vascular dementia was established by Two-vessel occlusion (2-VO) method, and cellular model of vascular dementia was established by oxygen glucose deprivation (OGD) method.
Phytother Res
January 2025
Department of Molecular and Developmental Medicine, School of Medicine, University of Siena, Polo Universitario San Miniato, Siena, Italy.
Drugs generally used in major depressive disorder are considered inappropriate for the more common milder forms. The efficacy of saffron extracts has been demonstrated in mild to moderate depression and in preclinical models of depression. However, evidence of saffron activity on reduced hedonic responsiveness and motivational anhedonia is limited.
View Article and Find Full Text PDFNeuropsychopharmacol Rep
March 2025
Department of Biology and Microbiology, Faculty of Medical Laboratory Technology, Khatam Al-Nabieen University, Kabul, Afghanistan.
Introduction: Substance use disorders, particularly alcohol use disorders, represent a significant public health problem, with adolescents particularly vulnerable to their adverse effects. This study examined the possible anxiolytic and antidepressant effects of biotin, a crucial vitamin for brain function, in attenuating the behavioral and neurobiological changes associated with alcohol withdrawal in adolescent rats.
Materials And Methods: Sixty male Sprague-Dawley rats were exposed to a 20% ethanol solution for 21 days, followed by a 21-day drug-free period to assess long-term behavioral and physiological changes.
J Neurochem
January 2025
Department of Neurology, Chang Gung Memorial Hospital, Chang Gung University College of Medicine, Taoyuan, Taiwan.
Misfolding and accumulation of amyloid-β (Aβ) in the brains of patients with Alzheimer's disease (AD) lead to neuronal loss through various mechanisms, including the downregulation of eukaryotic elongation factor 2 (EEF2) protein synthesis signaling. This study investigated the neuroprotective effects of indole and coumarin derivatives on Aβ folding and EEF2 signaling using SH-SY5Y cells expressing Aβ-green fluorescent protein (GFP) folding reporter. Among the tested compounds, two indole (NC009-1, -6) and two coumarin (LM-021, -036) derivatives effectively reduced Aβ misfolding and associated reactive oxygen species (ROS) production.
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