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
Infantile cerebral palsy (cerebral palsy) is one of the most common diseases of the nervoussystem in children. The etiology of cerebral palsy may differ, but structural changes in the brain in children are similar, regardless of clinical form. The paper summarizes the results of the recent studies on structural changes in the brain due to cerebral palsy. The literature sources demonstrate that the term of etiological factors impact on the developing brain of the fetus determines the characteristics of brain damage and localization of the damage, as well as the nature of the response from the nervous system.
Background. Up to the moment there is no universally accepted scheme of spatial organization of the groups of neurons of substantia nigra pars compacta of the human midbrain. A detailed study of the architectonics of this structure is necessary for pathomorphological analysis of agerelated changes in the nervous tissue and the associated neurodegenerative diseases with selective death of dopamine neurons.
Aim. To clarify the peculiarities of the morphochemical organization of the substantia nigra (SN) of a human brain and to create a threedimensional model of pars compacta.
Materials and Methods. Threedimensional reconstruction of substantia nigra pars compacta was performed on the brain autopsy material of individuals without neurological pathology (n=10, between 52 to 84 years of age) using a method of computed morphometry. Sections of the midbrain were stained by Nissl method and by an immunohistochemical method for localization of tyrosine hydroxylase – a marker of dopamine.
Results. In the SN pars compacta accumulations of neurons were identified in the form of 9 bands oriented in the rostrocaudal direction and including four areas: medial, lateral, dorsal and ventral. Morphometric analysis detected significant differences in the density of neurons and in expression of tyrosine hydroxylase between the areas of SN.
Conclusion. A model of cellular organization of SN pars compacta proposed by us on the basis of threedimensional reconstruction is characterized by a high degree of detalization as compared to similar works, and shows expressed spatial differentiation of the groups of neurons of SN which should be taken into consideration in pathomorphological examinations.
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