Androgens have a variety of protective and therapeutic effects in both the central and peripheral nervous systems. Here we review these effects as they related specifically to spinal and cranial motoneurons. Early in development, androgens are critical for the formation of important neuromuscular sex differences, decreasing the magnitude of normally occurring cell death in select motoneuron populations. Throughout the lifespan, androgens also protect against motoneuron death caused by axonal injury. Surviving motoneurons also display regressive changes to their neurites as a result of both direct axonal injury and loss of neighboring motoneurons. Androgen treatment enhances the ability of motoneurons to recover from these regressive changes and regenerate both axons and dendrites, restoring normal neuromuscular function. Androgens exert these protective effects by acting through a variety of molecular pathways. Recent work has begun to examine how androgen treatment can interact with other treatment strategies in promoting recovery from motoneuron injury.
Download full-text PDF |
Source |
---|---|
http://www.ncbi.nlm.nih.gov/pmc/articles/PMC2726741 | PMC |
http://dx.doi.org/10.1016/j.yfrne.2009.04.005 | DOI Listing |
Ann Neurol
January 2025
Department of Neurology, University of Massachusetts Chan Medical School, Worcester, MA.
ACS Chem Neurosci
January 2025
Department of Neurology, Multi-Omics Research Center for Brain Disorders,The First Affiliated Hospital, Hengyang Medical School, University of South China, Hengyang, Hunan 421001, China.
Brachial plexus root avulsion (BPRA) is often caused by road collisions, leading to total loss of motor function in the upper limb. At present, effective treatment options remain limited. Edaravone (EDA), a substance that eliminates free radicals, exhibits numerous biological properties, including neuroprotective, antioxidant and anti-inflammatory effects.
View Article and Find Full Text PDFPLoS One
January 2025
Department of Ophthalmology, Keck School of Medicine, USC Roski Eye Institute, University of Southern California, Los Angeles, California, United States of America.
Failure of central nervous system (CNS) axons to regenerate after injury results in permanent disability. Several molecular neuro-protective and neuro-regenerative strategies have been proposed as potential treatments but do not provide the directional cues needed to direct target-specific axon regeneration. Here, we demonstrate that applying an external guidance cue in the form of electric field stimulation to adult rats after optic nerve crush injury was effective at directing long-distance, target-specific retinal ganglion cell (RGC) axon regeneration to native targets in the diencephalon.
View Article and Find Full Text PDFJ Exerc Rehabil
December 2024
Department of Kinesiology, College of Natural Science, Jeju National University, Jeju, Korea.
The purpose of this study was to investigate the effects of weight- and non-weight-bearing exercises on the Basso-Beattie-Bresnahan (BBB) locomotor rating scale, corticospinal axon regrowth and regeneration-related proteins following spinal cord injury (SCI). Twenty-four male Sprague-Dawley rats were randomly divided into four groups: control group (n=6), SCI+sedentary group (SED, n=6), SCI+treadmill exercise group (TREAD, n=6), and SCI+swimming exercise group (SWIM, n=6). All rats in the SCI group were given the rest for 2 weeks after SCI, and then they were allowed to engage in low-intensity exercise for 6 weeks on treadmill device.
View Article and Find Full Text PDFNat Commun
January 2025
Institute of Developmental Biology and Neurobiology, Faculty of Biology, Johannes Gutenberg University Mainz, Mainz, Germany.
After a peripheral nerve injury, Schwann cells (SCs), the myelinating glia of the peripheral nervous system, convert into repair cells that foster axonal regrowth, and then remyelinate or re-ensheath regenerated axons, thereby ensuring functional recovery. The efficiency of this mechanism depends however on the time needed for axons to regrow. Here, we show that ablation of histone deacetylase 8 (HDAC8) in SCs accelerates the regrowth of sensory axons and sensory function recovery.
View Article and Find Full Text PDFEnter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!