Bone remodeling is thought to be regulated by many factors including nutritional status, humoral factors, and biomechanical stress. However, the involvement of the autonomic nervous system, mainly the sympathetic nervous system (SNS), in the modulation of bone remodeling is beginning to receive more attention. Neural innervation of bone has been demonstrated. Both experimental and clinical evidence has indicated the involvement of autonomic nervous system regulation in bone metabolism. The sympathetic neural pathway is so far the only identified link between the potent leptin-dependent central control and bone cells. An intact autonomic nervous system contributes to the maintenance of healthy bone tissue. Conversely, disturbance of the autonomic nervous system could induce abnormal bone remodeling. In this chapter, we review current knowledge about the role of the autonomic nervous system in abnormal bone formation and its association with clinical diseases such as heterotopic ossification, ossification of the posterior longitudinal ligament, postmenopausal osteoporosis, adolescent idiopathic scoliosis, complex regional pain syndrome, Charcot neuro-osteoarthropathy, unloading-induced osteoporosis, central or peripheral nervous system damage, and depression-induced osteoporosis. Understanding the mechanism of sympathetic neural signaling in bone remodeling may shed light on a potential treatment avenue for the prevention or reversal of bone loss.
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http://dx.doi.org/10.1016/B978-0-444-53491-0.00014-6 | DOI Listing |
Neurology
February 2025
Department of Advanced Biomedical Sciences, University "Federico II," Naples, Italy.
Background And Objectives: Although multiple sclerosis (MS) can be conceptualized as a network disorder, brain network analyses typically require advanced MRI sequences not commonly acquired in clinical practice. Using conventional MRI, we assessed cross-sectional and longitudinal structural disconnection and morphometric similarity networks in people with MS (pwMS), along with their relationship with clinical disability.
Methods: In this longitudinal monocentric study, 3T structural MRI of pwMS and healthy controls (HC) was retrospectively analyzed.
Science
January 2025
Department of Neuroscience, Karolinska Institutet, Stockholm, Sweden.
A previously unknown region in the brainstem controls dopamine activity.
View Article and Find Full Text PDFScience
January 2025
Laboratory of Cerebral Cortex Research, HUN-REN Institute of Experimental Medicine, Budapest, Hungary.
Rewards are essential for motivation, decision-making, memory, and mental health. We identified the subventricular tegmental nucleus (SVTg) as a brainstem reward center. In mice, reward and its prediction activate the SVTg, and SVTg stimulation leads to place preference, reduced anxiety, and accumbal dopamine release.
View Article and Find Full Text PDFAndrogens are pleiotropic and play pivotal roles in the formation and variation of sexual phenotypes. We show that differences in circulating androgens between the three male mating morphs in ruff sandpipers are linked to 17-beta hydroxysteroid dehydrogenase 2 (HSD17B2), encoded by a gene within the supergene that determines the morphs. Low-testosterone males had higher expression in blood than high-testosterone males, as well as in brain areas related to social behaviors and testosterone production.
View Article and Find Full Text PDFPLoS Biol
January 2025
Department of Neurology, School of Medicine and Health, Technical University of Munich (TUM), Munich, Germany.
Pain is closely linked to alpha oscillations (8 < 13 Hz) which are thought to represent a supra-modal, top-down mediated gating mechanism that shapes sensory processing. Consequently, alpha oscillations might also shape the cerebral processing of nociceptive input and eventually the perception of pain. To test this mechanistic hypothesis, we designed a sham-controlled and double-blind electroencephalography (EEG)-based neurofeedback study.
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