Alzheimer's disease (AD) is characterized by a progressive decline in cognitive function; however, recent evidence suggests that non-cognitive sensorimotor and psychomotor symptoms accompany early stages of the disease in humans and AD models. Although exercise is emerging as an important therapeutic to combat AD progression, little is known about the effect of exercise on sensorimotor domain functions. The purpose of this study was to determine if early sensorimotor symptoms accompany deficits in Morris water maze (MWM) performance in the 3xTg-AD model, and investigate if exercise could protect against early behavioral decline.
View Article and Find Full Text PDFBackground: Adequate pain education of health professionals is fundamental in the management of pain. Although an interprofessional consensus of core competencies for health professional pre-licensure education in pain have been established, the degree of their incorporation into physical therapy curriculum varies greatly. The purpose of this study was to 1.
View Article and Find Full Text PDFDiabetic peripheral neuropathy (DPN) occurs in more than 50% of people with diabetes and is an important risk factor for skin breakdown, amputation, and reduced physical mobility (ie, walking and stair climbing). Although many beneficial effects of exercise for people with diabetes have been well established, few studies have examined whether exercise provides comparable benefits to people with DPN. Until recently, DPN was considered to be a contraindication for walking or any weight-bearing exercise because of concerns about injuring a person's insensitive feet.
View Article and Find Full Text PDFExercise has been shown to protect against cognitive decline and Alzheimer's disease (AD) progression, however the dose of exercise required to protect against AD is unknown. Recent studies show that the pathological processes leading to AD cause characteristic alterations in blood and brain inflammatory proteins that are associated with the progression of AD, suggesting that these markers could be used to diagnosis and monitor disease progression. The purpose of this study was to determine the impact of exercise frequency on AD blood chemokine profiles, and correlate these findings with chemokine brain expression changes in the triple transgenic AD (3xTg-AD) mouse model.
View Article and Find Full Text PDFBackground: Neuropathic pain and sensory abnormalities are a debilitating secondary consequence of spinal cord injury (SCI). Maladaptive structural plasticity is gaining recognition for its role in contributing to the development of post SCI pain syndromes. We previously demonstrated that excitotoxic induced SCI dysesthesias are associated with enhanced dorsal root ganglia (DRG) neuronal outgrowth.
View Article and Find Full Text PDFSensory dysesthesias and pain are common sequelae following spinal cord injury (SCI). While efforts to understand the mechanisms involved in SCI pain syndromes have focused on spinal and supraspinal regions, recent evidence suggests that SCI induces pathological responses in primary afferent neurons that may contribute to the development of sensory abnormalities. The purpose of this study was to investigate if excitotoxic spinal lesions lead to abnormal growth responses of cultured dorsal root ganglia (DRG) neurons, and to examine if the degree of neurite growth correlated with the presence of dysesthesias.
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