Objective: To evaluate motor function in men with spinal cord injury (SCI) given testosterone replacement therapy (TRT).
Design: American Spinal Injury Association (ASIA) rehabilitation discharge motor index scores were compared between men with SCI given TRT (testosterone cypionate, 200 mg, monthly; n = 50) and a comparison group (n = 480) in a retrospective study. Covariates included admission motor and FIM scores, level of injury (paraplegia/tetraplegia), days since injury, and age.
Results: ASIA discharge motor scores for ASIA impairment scale grades C and D were significantly different (P < 0.05) in men with incomplete SCI given TRT, relative to the comparison group. The covariate-adjusted mean discharge score for the TRT group was higher than for the comparison group. There were no significant differences in discharge FIM scores (P = 0.34) for men with incomplete injuries and no differences in the adjusted discharge ASIA motor scores (P = 0.92) or adjusted discharge FIM scores (P = 0.16) for men with complete injuries.
Conclusion: The data support a relationship between TRT and strength gains in men with residual motor function after SCI. Prospective studies are necessary to validate these findings.
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http://dx.doi.org/10.1097/PHM.0b013e318168bbec | DOI Listing |
Lab Anim Res
January 2025
Anatomy Department, Faculty of Basic Medical Sciences, Alex Ekwueme, Federal University, Ndufu-Alike, Ebonyi State, Nigeria.
Background: The Microtubules-associated protein tau (MAPT), alpha-synuclein (SNCA), and leucine zipper tumor suppressor 3 (LZTS3) genes are implicated in neurodegeneration and tumor suppression, respectively. This study investigated the regulatory roles of eugenol on paraquat-altered genes.
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BMC Med Genomics
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Sheffield Institute for Translational Neuroscience (SITraN), University of Sheffield, Sheffield, UK.
Amyotrophic lateral sclerosis (ALS) lacks a specific biomarker, but is defined by relatively selective toxicity to motor neurons (MN). As others have highlighted, this offers an opportunity to develop a sensitive and specific biomarker based on detection of DNA released from dying MN within accessible biofluids. Here we have performed whole genome bisulfite sequencing (WGBS) of iPSC-derived MN from neurologically normal individuals.
View Article and Find Full Text PDFProbiotics Antimicrob Proteins
January 2025
Department of Pharmacology and Toxicology, National Institute of Pharmaceutical Education and Research, S.A.S. Nagar, Mohali, Punjab, 160062, India.
Recent evidence links gut microbiota alterations to neurodegenerative disorders, including Parkinson's disease (PD). Replenishing the abnormal composition of gut microbiota through gut microbiota-based interventions "prebiotics, probiotics, synbiotics, postbiotics, and fecal microbiota transplantation (FMT)" has shown beneficial effects in PD. These interventions increase gut metabolites like short-chain fatty acids (SCFAs) and glucagon-like peptide-1 (GLP-1), which may protect dopaminergic neurons via the gut-brain axis.
View Article and Find Full Text PDFNPJ Parkinsons Dis
January 2025
Aligning Science Across Parkinson's (ASAP) Collaborative Research Network, Chevy Chase, MD, 20852, USA.
ΑBSTRACT: In Parkinson's disease (PD), Lewy pathology deposits in the cerebral cortex, but how the pathology disrupts cortical circuit integrity and function remains poorly understood. To begin to address this question, we injected α-synuclein (αSyn) preformed fibrils (PFFs) into the dorsolateral striatum of mice to seed αSyn pathology in the cortical cortex and induce degeneration of midbrain dopaminergic neurons. We reported that αSyn aggregates accumulate in the motor cortex in a layer- and cell-subtype-specific pattern.
View Article and Find Full Text PDFCell Death Dis
January 2025
NMPA Key Laboratory for Research and Evaluation of Narcotic and Psychotropic Drugs, Xuzhou, China.
Neuroinflammation is a key factor in the pathogenesis of Parkinson's disease (PD). Activated microglia in the central nervous system (CNS) and infiltration of peripheral immune cells contribute to dopaminergic neuron loss. However, the role of peripheral immune responses, particularly triggering receptor expressed on myeloid cells-1 (TREM-1), in PD remains unclear.
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