ABSTRACT
The formation mechanism of amyloid peptides in normally functioning neuron and upon the development of amyloidosis resulting in neuron death is described. Amyloid peptides are formed by enzymatic processing of a large protein precursor and participate in intermolecular interactions after conformational rearrangements resulting in the formation of pathogenic structures. They enter into the cascade of molecular and cellular events leading to amyloidosis and death of nervous cells. These molecular events clarify the relation between the conformation and function of neuropathogenic peptides and the role of this relation in the development of pathology of differentiated neurons. The English version of the paper: Russian Journal of Bioorganic Chemistry, 2006, vol. 32, no. 3; see also http://www.maik.ru.
Subject(s)
Amyloid beta-Peptides/metabolism , Amyloidosis/metabolism , Neurons/metabolism , Peptides/metabolism , Amyloid beta-Peptides/genetics , Amyloidosis/genetics , Amyloidosis/pathology , Animals , Cell Death , Cell Differentiation , Humans , Neurons/pathology , Peptides/geneticsABSTRACT
A conception on amyloidosis as a key factor of neuronal death in neurodegenerative diseases is stated. Experimental evidence is presented that amyloidosis is caused by alterations in the activity of a number of enzymes as well as conformational changes in pathogenic proteins. Arguments for amyloidosis as the universal biological mechanism of specific elimination of neurons showing changed metabolic and physiological status of cell differentiation are adduced. The final pattern of cell death seems to differ cardinally from that in both apoptosis and necrosis.
Subject(s)
Amyloid/metabolism , Amyloidosis/metabolism , Apoptosis , Necrosis , Neurodegenerative Diseases/metabolism , Neurons/metabolism , Humans , Protein ConformationABSTRACT
Sera of 80 patients with pyodermias of varius etiology were analysed for interferon-gamma (IF-gamma), antiinterferon autoantibodies (IF-a-AB), corresponding antiidiotypic antibodies (IF-AIAB) and the ratio IF-a-AB/IF-AIAB using ELISA assay. There was no correlation between serum IF-gamma and IF-a-AB. Progression of this disease was characterized by an increase of serum IF-a-AB and a decrease of IF-AIAB. Prolonged duration of this disease also caused the decrease of serum anti IF-a-AB and IF-AIAB. The ratio of IF-a-AB/IF-AIAB increased with severity and duration of this disease.
