The article reviews the literature on copper and zinc level alterations in the brain structures in neurodegenera-tive diseases (Parkinson's disease, PD, and Alzheimer's disease, AD). We discuss the ability of these micro-elements to bind to cellular proteins (α-synuclein in PD and β-amyloid in AD) disrupting their metabolism. The literature analysis shows that high copper levels in the neurons of nigrostriatal brain formations in PD initiate oxidative stress development. Copper extracellular deficiency disturbs iron metabolism and thus may increase the stress. Low zinc levels weaken the enzyme antioxidant potential. In AD, disruption of the homeostasis of these metals in the brain structures has a different effect. In the early stages, the complex formed by β-amyloid and copper (II) ions is involved in a series of redox reactions, resulting in the formation of free radicals which stimulate the expression of neuroinflammatory mediator, accompanied by uncontrolled release of zinc, high concentrations of which catalyzing the formation of the toxic forms of aggregated Aβ.
Keywords: brain, copper, zinc, Parkinson’s disease, Alzheimer’s disease
The effects of activated protein C (APC) on the quantitative parameters of neurons and neuroglia in the perifocal zone of infarction induced in the left hemispheric cortex were studied in two groups of rats. Group 1 animals served as control (control infarction). Group 2 rats were injected with APC (50 μg/kg) in the right lateral cerebral ventricle 3 h after infarction was induced, and after 72 h the infarction size was evaluated and the neurons and neuroglia in the perifocal zone were counted. APC reduced the infarction size 2.5 times in comparison with the control and reduced by 16% the neuronal death in the perifocal zone layer V, causing no appreciable changes in layer III, and did not change the size of neuronal bodies but increased (by 11%) the size of neuronal nuclei in layer III. The protein maintained the sharply increased count of gliocytes in the perifocal zone of infarction and promoted their growth. Hence, APC protected the neurons from death in the ischemic focus by increasing the gliocyte count and stimulating the compensatory reparative processes.
Purpose of the study: to study the neurological status, anamnesis data and electroencephalography in patients with autism spectrum disorders.Material and methods. The study involved 54 children with autism spectrum disorders aged from 3 to 7 years. Anamnestic data were studied, neurological and electroencephalographic studies were performed.Results. The following were identified as the main antenatal and intranatal risk factors for the formation of neurological disorders: gestosis, the threat of termination of pregnancy, weakness of labor and an increase in the duration of the anhydrous period in mothers. A significant number of children were born prematurely and had signs of intrauterine hypoxia at birth. When examining the neurological status, the majority of patients revealed motor and coordination disorders, disorders of tactile sensitivity. Electroencephalography made it possible to register in most patients a delay in the formation of the rhythm of the bioelectrical activity of the brain. Periodic regional decelerations were detected in 9 cases, and epileptiform activity — in 5 cases.Conclusion. Disorders in the neurological status in children with autism spectrum disorders were noted in the form of mild motor symptoms, disorders of motor coordination and tactile sensitivity.
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