Temirbolat T Berezov

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Several previous studies reported the association of the soluble form of amyloid beta (sA beta) protein, a major constituent of amyloid deposits in Alzheimer's disease (AD), with normal blood, cerebrospinal fluid (CSF) and central nervous system high density lipoproteins (HDLs). The present report aimed to elucidate the pattern of sA beta and apolipoprotein(More)
The Abeta-amyloid peptide (Abeta), the main component of amyloid plaques, is derived by proteolytic cleavage from the amyloid precursor protein (APP). Epidemiologic and biochemical data suggest a link between cholesterol, APP processing, Abeta, and Alzheimer's disease. Two recent epidemiologic studies indicate that there is a decreased prevalence of AD(More)
The importance of homeostasis of neural tissue to neuron functioning, the synaptic plasticity of the hippocampus, and laboratory animals' behavior was demonstrated by the authors earlier. A range of experimental data evidences that cholinergic neurotransmission, ionotropic and metabotropic receptors, excessive tau phosphorylation, alterations in(More)
Despite a decade long universal publication in favor of the view on amyloid-beta (A beta) as Alzheimer's disease culprit (solely neurotoxic for neurons and brain tissue), current scientific evidence leaves little doubt that A beta serves an essential role at synapse and in synaptic structure-functional plasticity that underlie learning and memory.(More)
This review considers some aspects of the biochemistry of beta-amyloid, a protein which produces insoluble deposits in the brain. These deposits are a specific morphological feature of Alzheimer's disease, Down's syndrome, and senile dementia. Our contribution to the concept of a soluble form of beta-amyloid as of a normal human protein is presented.
In this review, we propose that the neurodegenerative changes in the neurochemistry of amyloid-beta (Abeta) aggregation, tau phosphorylation, cytoskeleton rearrangement, oxidative stress, and lipid peroxidation in Alzheimer's disease (AD), and a number of other neurodegenerative diseases, are secondary pathological features. In fact, we believe that these(More)
We studied the expression of peroxiredoxin genes (PRDX1, PRDX2, PRDX3, and PRDX6) in human erythroleukemia K652, human breast carcinoma MCF-7, and human ovarian carcinoma SKOV-3 cells during cisplatin resistance development. It was found that drug resistance formation was accompanied by a significant increase in the expression of PRDX1, PRDX2, PRDX3, PRDX6(More)
In-depth scholar literature analysis of Alzheimer's disease neurodegenerative features of amyloid beta protein neurochemistry modification and excessive phosphorylation of tau protein (and associated neuronal cytoskeleton rearrangements) are secondary phenomena. At early disease stage these neurobiochemical mechanisms are reversible and serve to heal an(More)
During a decade there was a dogma that Alzheimer's amyloid beta (Ap) is produced only upon the disease, and that this protein is neurotoxic for neurons and brain tissue. Current scientific evidence demonstrate that AP is an essential molecule in synaptic plasticity that underlie learning and memory. Therefore, it was hypothesized that the change of AP(More)