Impact of nutrition on inflammation, tauopathy, and behavioral outcomes from chronic traumatic encephalopathy
| Autor: | Stephen Perry, Saeid Taheri, Mark S. Kindy, Hong Zhu, William Mondy, Jin Yu |
|---|---|
| Rok vydání: | 2018 |
| Předmět: |
0301 basic medicine
Male Pathology Concussion Behavioral Symptoms lcsh:RC346-429 Mice 0302 clinical medicine Brain Injuries Traumatic Chronic traumatic encephalopathy Trauma Severity Indices Microglia biology Glial fibrillary acidic protein General Neuroscience Neurodegeneration Astrogliosis medicine.anatomical_structure Neurology Hindlimb Suspension Tauopathies Cytokines Tauopathy medicine.medical_specialty Immunology Tau protein Spatial Learning Mice Transgenic tau Proteins Pathophysiology 03 medical and health sciences Cellular and Molecular Neuroscience Risk-Taking medicine Animals Humans Animal model Muscle Strength lcsh:Neurology. Diseases of the nervous system Swimming Repetitive Inflammation business.industry Nutrients medicine.disease Diet Disease Models Animal 030104 developmental biology biology.protein business Sleep 030217 neurology & neurosurgery |
| Zdroj: | Journal of Neuroinflammation, Vol 15, Iss 1, Pp 1-16 (2018) |
| ISSN: | 1742-2094 |
| Popis: | Background Repetitive mild traumatic brain injuries (rmTBI) are associated with cognitive deficits, inflammation, and stress-related events. We tested the effect of nutrient intake on the impact of rmTBI in an animal model of chronic traumatic encephalopathy (CTE) to study the pathophysiological mechanisms underlying this model. We used a between group design rmTBI closed head injuries in mice, compared to a control and nutrient-treated groups. Methods Our model allows for controlled, repetitive closed head impacts to mice. Briefly, 24-week-old mice were divided into five groups: control, rmTBI, and rmTBI with nutrients (2% of NF-216, NF-316 and NF-416). rmTBI mice received four concussive impacts over 7 days. Mice were treated with NutriFusion diets for 2 months prior to the rmTBI and until euthanasia (6 months). Mice were then subsequently euthanized for macro- and micro-histopathologic analysis for various times up to 6 months after the last TBI received. Animals were examined behaviorally, and brain sections were immunostained for glial fibrillary acidic protein (GFAP) for astrocytes, iba-1 for activated microglia, and AT8 for phosphorylated tau protein. Results Animals on nutrient diets showed attenuated behavioral changes. The brains from all mice lacked macroscopic tissue damage at all time points. The rmTBI resulted in a marked neuroinflammatory response, with persistent and widespread astrogliosis and microglial activation, as well as significantly elevated phospho-tau immunoreactivity to 6 months. Mice treated with diets had significantly reduced inflammation and phospho-tau staining. Conclusions The neuropathological findings in the rmTBI mice showed histopathological hallmarks of CTE, including increased astrogliosis, microglial activation, and hyperphosphorylated tau protein accumulation, while mice treated with diets had attenuated disease process. These studies demonstrate that consumption of nutrient-rich diets reduced disease progression. |
| Databáze: | OpenAIRE |
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