[Morphochemical study of alpha-synuclein, iron and iron-containing proteins in the substantia nigra of the brain in Parkinson's disease]. / Morfokhimicheskoe issledovanie al'fa-sinukleina, zheleza i zhelezosoderzhashchikh belkov v chernom veshchestve golovnogo mozga pri bolezni Parkinsona.

OBJECTIVE: To study, using a complex morphochemical approach, the localization of alpha-synuclein, iron compounds and iron-containing proteins in the structures of the substantia nigra of the brain in Parkinson's disease (PD). MATERIAL AND METHODS: Histochemistry and immunohistochemistry methods have been used to study the localization of pathological alpha-synuclein (α-Syn-p129), iron compounds and iron-containing proteins - transferrin receptor and ferritin in neurons and neuroglia in the substantia nigra of the brain of deceased PD patients and persons with no neurological symptoms detected during life (control). RESULTS: In the substantia nigra of PD patients, in comparison with the control, a stable accumulation of pathological alpha-synuclein (α-Syn-p129) in the bodies and processes of neurons was found, and in the neuroglia and neuropil - the accumulation of iron (II) and ferritin heavy chain, the reaction of microglia to protein CD68 was moderately elevated. The transmembrane protein CD71 was detected equally in the brains of PD patients and in controls. CONCLUSION: Synaptic protein alpha-synuclein in PD turns into a pathological metabolite that accumulates in the structures of substantia nigra, and probably disrupts the conduction of nervous excitation. Excessive accumulation of the ferritin heavy chain in neuroglia can increase the concentration of reactive forms of iron and increase neurotoxicity. The uniform distribution of the transmembrane glycoprotein CD71 in the of substantia nigra structures both in the control and in PD patients indicates the preservation of non-heme iron transport during the neurodegenerative process.

[The role of aluminum and lead in the development of Alzheimer's and Parkinson's diseases]. / Rol' alyuminiya i svintsa v razvitii boleznei Al'tsgeimera i Parkinsona.

The article summarizes the data available in the literature on the toxic effects of aluminum and lead on the human brain and assesses the relationship of these effects to the etiopathogenesis of the most common neurodegenerative diseases, such as Alzheimer's and Parkinson's diseases. The accumulation of ions of these metals in the brain structures leads to chronic intoxication that is manifested by the morphological signs that are typical for Alzheimer's disease, such as deposits of ß-amyloid and τ-protein mainly in the frontal and temporal regions of the cortex, and for Parkinson's disease, such as degeneration of dopamine neurons in the substantia nigra and their accumulation of α-synuclein. The most likely forms of participation of aluminum and lead ions in the mechanisms of neurodegeneration are the replacement of bivalent metal ions necessary for brain functioning, oxidative stress initiation, epigenetic modifications of histones, and increased expression of noncoding ribonucleic acids.

Immunohistochemical Assessment of the Compensatory Responses in Rat Olfactory Bulbs after 6-Hydroxydopamine-Induced Lesion of the Substantia Nigra.

We assessed changes of olfactory bulbs in rata with 6-hydroxydopamine destruction of the substantia nigra. The expression of marker proteins of immature and differentiated neurons and glia (vimentin, PSA-NCAM, tyrosine hydroxylase, and S100) was analyzed by immunohistochemical and morphometric methods. The number of periglomerular dopamine neurons and astroglia in the olfactory bulbs increased on the side of toxin injection and expression of PSA-NCAM and vimentin increased in the rostral migratory stream. Destruction of the substantia nigra shifted differentiation of neuronal progenitors towards the dopaminergic phenotype and increased their survival in the olfactory bulbs, which can be explained by increased expression of PSA-NCAM.

Quantitative assessment of neurons and neuroglia with computer morphometry.

The morphology of neural and glial cells in different cerebral areas and in various experimental models was quantitatively studied by methods of computer morphometry combined with video image analysis systems. The following parameters were obtained: density of neurons and glial cells per 1 mm(2), number of satellite perineuronal glial cells, aspect ratio for neural and glial cells, the area occupied by neuroglial projections, etc. The tested computer morphometry methods can be efficient in quantitative assessment of pathological and regenerative processes in the nervous tissue.

Effect of delta-sleep-inducing peptide on activity of enzymes of biogenic amine metabolism in the brain of Wistar and August rats.

Activity of enzymes catalyzing synthesis and degradation of serotonin and dopamine in brain structures of Wistar and August rats was measured biochemically under normal conditions and after short-term exposure to delta-sleep-inducing peptide. The effects of the test peptide manifested in activation of the serotoninergic system and inhibition of the dopaminergic system, particularly in the caudate nucleus. These changes were most pronounced in the brain of Wistar rats.

Lysosomal proteinases as putative diagnostic tools in human neuropathology: Alzheimer disease (AD) and schizophrenia.

The cathepsin B, D and L were studied by immunohistochemical techniques in the human postmortem brain. The enzyme were primarily localized in neurons. Makroglial cells were seldom immunostained. It is shown that cathepsins B and D frequently occur in neuritic plaques of Alzheimer victims, thereby raising the question, whether or not cathepsin immunohistochemistry is a useful tool in the diagnosis of this disease. Furthermore, we identified certain glial cells to be immunoreactive for cathepsins in schizophrenics.