Intensive protein synthesis in neurons and phosphorylation of beta-amyloid precursor protein and tau-protein are triggering factors of neuronal amyloidosis and Alzheimer's disease

   
Maltsev A.V.1 , Dovidchenko N.V.2, Uteshev V.K.3, Sokolik V.V.4, Shtang O.M.5, Yakushin M.A.6, Sokolova N.M.6, Surin A.K.7, Galzitskaya O.V.2

1. Russian Gerontological Research Clinical Center, Russian Ministry of Health Care; Institute of Theoretical and Experimental Biophysics, Russian Academy of Sciences
2. Insitute of Protein Research, Russian Academy of Sciences
3. Institute of Biophysics Cell, Russian Academy of Sciences
4. Institute of Neurology, Psychiatry and Addiction Medical Sciences of Ukraine
5. MDSICI M.F. Vladimirsky
6. Russian Gerontological Research Clinical Center, Russian Ministry of Health Care
7. Insitute of Protein Research, Russian Academy of Sciences; State Research Center for Applied Microbiology & Biotechnology
Section: Review
DOI: 10.18097/pbmc20135902144      UDK: 577.32.4.322+616.003.821+616.831      PubMed Id: 23789343
Year: 2013  Volume: 59  Issue: 2  Pages: 144-170
Recently the studies of Alzheimer’s disease have become particularly actual and have attracted scientists from all over the world to this problem as a result of dissemination of this dangerous disorder. The reason for such pathogenesis is not known, but the final image, for the first time obtained on microscopic brain sections from patients with this disease more than a hundred years ago, is well known to clinicists. This is the deposition of Ab amyloid in the brain tissue of senile plaques and fibrils. Many authors suppose that the deposition of beta-amyloid provokes secondary neuronal changes which are the reason of neuron death. Other authors associate the death of neurons with hyperphosphorylation of tau-proteins which form neurofibrillar coils inside nerve cells and lead to their death. For creation of methods of preclinical diagnostics and effective treatment of Alzheimer’s disease novel knowledge is required on the nature of triggering factors of sporadic isoforms of Alzheimer’s disease, on cause-effect relationships of phosphorylation of amyloid precursor protein with formation of pathogenic beta-amyloids, on the relationship with these factors of hyperphosphorylation of tau-protein and neuron death. In this review we analyze the papers describing the increasing of intensity of biosynthesis in neurons in normal conditions and under the stress, the possibility of development of energetic unbalanced neurons and activation of their protective systems. Phosphorylation and hyperphosphorylation of tau-proteins is also tightly connected with protective mechanisms of cells and with processes of evacuation of phosphates, adenosine mono-phosphates and pyrophosphates from the region of protein synthesis. Upon long and high intensity of protein synthesis the protective mechanisms are overloaded and the complementarity of metabolitic processes is disturbed. This results in dysfunction of neurons, transport collapse, and neuron death.
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Maltsev A.V., Dovidchenko N.V., Uteshev V.K., Sokolik V.V., Shtang O.M., Yakushin M.A., Sokolova N.M., Surin A.K., Galzitskaya O.V. (2013) Biomeditsinskaya khimiya, 59(2), 144-170.
This paper is also available as the English translation:10.1134/S1990750813040057
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