Publications by authors named "P Popovich"
. Macrophages and astrocytes play a crucial role in the aftermath of a traumatic spinal cord injury (SCI). Infiltrating macrophages adopt a pro-inflammatory phenotype while resident astrocytes adopt a neurotoxic phenotype at the injury site, both of which contribute to neuronal death and inhibit axonal regeneration.
View Article and Find Full Text PDFRobust structural remodeling and synaptic plasticity occurs within spinal autonomic circuitry after severe high-level spinal cord injury (SCI). As a result, normally innocuous visceral or somatic stimuli elicit uncontrolled activation of spinal sympathetic reflexes that contribute to systemic disease and organ-specific pathology. How hyperexcitable sympathetic circuitry forms is unknown, but local cues from neighboring glia likely help mold these maladaptive neuronal networks.
View Article and Find Full Text PDFArticle Synopsis
- * SCI individuals face a higher risk of severe diabetes and cardiovascular diseases compared to the general population, leading to potentially life-threatening complications such as strokes and heart attacks.
- * Research comparing lean rats with SCI to obese rats shows that SCI can produce MetS symptoms that are equal to or more severe than those seen in diet-induced obesity, emphasizing the complex metabolic challenges faced by individuals with SCI, especially if they were obese prior to the injury.
Article Synopsis
- Spinal cord injury (SCI) leads to issues with motor and sensory functions, and often results in gut problems like gastrointestinal complications and neurogenic bowel, affecting quality of life.
- Research shows that high cervical SCI causes temporary gut imbalance (dysbiosis) which contributes to ongoing GI issues and hinders recovery.
- Probiotic treatment can improve gut health and respiratory function post-SCI by reducing inflammation and enhancing nerve regeneration, highlighting the gut microbiome's potential as a treatment target for better recovery.
An incomplete mechanistic understanding of skeletal muscle wasting early after spinal cord injury (SCI) precludes targeted molecular interventions. Here, we demonstrated systemic wasting that also affected innervated nonparalyzed (supralesional) muscles and emerged within 1 week after experimental SCI in mice. Systemic muscle wasting caused muscle weakness, affected fast type 2 myofibers preferentially, and became exacerbated after high (T3) compared with low (T9) thoracic paraplegia, indicating lesion level-dependent ("neurogenic") mechanisms.
View Article and Find Full Text PDF