Abstract
Increased interest regarding the biometal mechanisms of action and the pathways in which they have regulatory roles was lately observed. Particularly, it was shown that biometal homeostasis dysregulation may lead to neurodegeneration including Alzheimer's disease, Parkinson disease, or prion protein disease, since important molecular signaling mechanisms in brain functions implicate both oxidative stress and redox active biometals. Oxidative stress could be a result of a breakdown in metal-ion homeostasis which leads to abnormal metal protein chelation. In our previous work, we reported a strong correlation between Alzheimer's disease and oxidative stress. Consequently, the aim of the present work was to evaluate some of the biometals' levels (magnesium, manganese, and iron), the specific activity of some antioxidant enzymes (superoxide dismutase and glutathione peroxidase), and a common lipid peroxidation marker (malondialdehyde concentration), in mild cognitive impairment (n = 15) and Alzheimer's disease (n = 15) patients, compared to age-matched healthy subjects (n = 15). We found increased lipid peroxidation effects, low antioxidant defense, low magnesium and iron concentrations, and high manganese levels in mild cognitive impairment and Alzheimer's disease patients, in a gradual manner. These data could be relevant for future association studies regarding the prediction of Alzheimer's disease development risk or circling through stages by analyzing both active redox metals, oxidative stress markers, and the correlations in between.
Highlights
It is generally accepted that several biometals (BM) such as iron, copper, zinc, manganese, and magnesium are vital in the complex cellular activities and regulation [1,2,3,4,5]
We observed an iron levels decrease in the Alzheimer’s disease (AD) patients sera (140.43 ± 16.02 μg/dl) as compared with the healthy sex- and age-matched controls (192.45 ± 42.51 μg/dl)
We firstly observed a slight increase of the iron levels in the mild cognitive impairment (MCI) patients (242.47 ± 18.06 μg/dl) followed by the significant decrease in AD patients (Figure 1)
Summary
It is generally accepted that several biometals (BM) such as iron, copper, zinc, manganese, and magnesium are vital in the complex cellular activities and regulation [1,2,3,4,5]. AD is a complex disorder involving both behavioral and molecular distress In this way, it is accepted that AD is a multifactorial disease in which several important components have been described: the discrete biochemical changes which firstly occur triggering cellular modifications such as amyloid accumulation and neurofibrillary tangles formation; the histological typical features accompanied by synaptic disruption and neuronal loss; and last but not the least the visible symptoms of the behavioral component—memory loss, cognitive decline, and related comorbidities (affective distress and somatic disorders such as chronic pain or anemia) [6,7,8,9]. While some overlapping traits between MCI and the early stages of AD in considering the characteristic mild cognitive decline were suggested, it was shown that AD cognitive abilities gradually decline, but MCI patients’ cognitive state remains stable for years [10]
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