Alzheimer's disease is a highly prevalent disease in the elderly, characterized by degeneration of brain tissue that can lead to impairment of cognitive domains, progressive loss of memory, dementia and death. The formation of extracellular senile plaques from beta-amyloid peptides and the hyperphosphorylation of the tau protein provoke destabilization of the neuronal support network, causing neuronal inflammation and decreased synaptic activities. Studies have shown that peripheral organs can make a significant contribution to the clearance of beta-amyloid peptides and, moreover, show a relationship between the deficiency of this peripheral system and its contribution to the pathogenesis of Alzheimer's disease. Therefore, there is an indication that this clearance mechanism may have a therapeutic and preventive potential for pathology. In this context, it is suggested that the organs responsible for the uptake of the beta-amyloid peptides in the blood are the liver and the kidney, including data point to an abnormal hepatic accumulation of beta-amyloid peptides. It is also known that these peptides can cause damage to mitochondria, exerting their toxicity intracellularly. In addition to supplying most of the ATP required for cellular functions, mitochondria also play an important role in calcium homeostasis and regulation of programmed cell death. Since mitochondrial functions are of great importance for the interpretation of several processes that govern energy metabolism within the complex intracellular network in hepatocytes and the relevance that hepatic tissue may have on mechanisms involved with beta-amyloid peptides, this work aims to analyze parameters of the mitochondrial bioenergetics of this tissue and to establish its relationship with Alzheimer's disease. To do so, experiments will be performed to verify if there is hepatic dysfunction in an experimental model for Alzheimer's disease, with emphasis on changes in mitochondrial functions.
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