ABSTRACT
Traumatic spinal cord injuries (SCI) result in devastating impairment to an individual's functional ability. The pathophysiology of SCI is related to primary injury but further propagated by secondary reactions to injury, such as inflammation and oxidation. The inflammatory and oxidative cascades ultimately cause demyelination and Wallerian degeneration. Currently, no treatments are available to treat primary or secondary injury in SCI, but some studies have shown promising results by lessening secondary mechanisms of injury. Interleukins (ILs) have been described as key players in the inflammation cascade after neuronal injury; however, their role and possible inhibition in the context of acute traumatic SCIs have not been widely studied. Here, we review the relationship between SCI and IL-6 concentrations in the CSF and serum of individuals after traumatic SCIs. Furthermore, we explore the dual IL-6 signaling pathways and their relevance for future IL-6 targeted therapies in SCI.
ABSTRACT
It is well-documented that when mercury levels surpass the permissible value, individuals experience a myriad of symptoms that include chronic fatigue, dizziness, and loss of appetite. Mercury is also known to be one of the most potent neurotoxins. This case study depicts a 91- year-old who presented with cognitive decline diagnosed as Alzheimer's disease. This patient was found to have severely elevated mercury levels caused by consuming high mercury containing fish. Following diet adjustment and detoxification, this patient's cognitive impairment significantly improved in proportion to the decline in methylmercury level. One year later, his cognition and functional status rapidly and unexpectedly declined. A computed tomography (CT) scan revealed multiple new lacunar subacute strokes. Thus, it is critical to address biological etiologies such as mercury toxicity in the elderly population diagnosed with Alzheimer's, but end organ damage may not be reversible.
