Abstract

The aim of this study was to qualitatively described effect of the oxidative stress, neurotransmission change and the neurodegeneration in animal model of chronic intoxication by aluminum. Electrocortical brain activity of animal model of stress and neurodegeneration is comparable with Alzheimer’s Dementia (AD). We used adult animals, during 6 weeks intraperitoneally treated with aluminum. Both animals and patients with Alzheimer’s Dementia have increased relative spectral power in delta range. By fractal analysis we described changes in electrocortical activity of aluminum intoxication animals compare to physiological control. We used change in delta range to calculate fractal dimension for the pathophysiological state of disease. We evaluate effect of stress and neurodegeneration, oxidative stress and accumulation of beta amyloid and neurofibrillary tangles as change in fractal dimension (FD). We conclude that change in fractal dimension could be used for prognosis of AD. Results show that decrease in fractal dimension could be used for evaluation of changes in neural activity in occurrence of AD.

Highlights

  • Alzheimer’s disease is characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-β containing plaques and neurofibrillary tangles

  • We evaluate effect of stress and neurodegeneration, oxidative stress and accumulation of beta amyloid and neurofibrillary tangles as change in fractal dimension (FD)

  • We can conclude that stress and neurodegeneration as primary events of neurotoxicity in aging and occurrence of beta amyloid and neurofibrilary tangles as secondary effect, both have decreased fractal dimension. Both events are responsible for development of Alzheimer’s disease. This animal model is convenient because stress and neurodegeneration have synergistic effect in diagnosis and prognosis of Alzheimer’s Dementia

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Summary

Introduction

Alzheimer’s disease is characterized by cognitive impairment, progressive neurodegeneration and formation of amyloid-β containing plaques and neurofibrillary tangles. The neurodegenerative process in AD is characterized by synaptic damage accompanied by neuronal loss. Pathology of synapses and defective neurogenesis in AD are related to progressive accumulation of Aβ resulting in the formation of toxic oligomers.

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