Academic Journal
Molecular expression of insulin signal transduction components in brain cells in an experimental model of Alzheimer’s disease
| العنوان: | Molecular expression of insulin signal transduction components in brain cells in an experimental model of Alzheimer’s disease |
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| المؤلفون: | Yana V. Gorina, Yuliya K. Komleva, Olga L. Lopatina, Anatolii I. Chernykh, Alla B. Salmina |
| المصدر: | Анналы клинической и экспериментальной неврологии, Vol 13, Iss 4, Pp 28-37 (2019) |
| بيانات النشر: | Research Center of Neurology, 2019. |
| سنة النشر: | 2019 |
| المجموعة: | LCC:Neurosciences. Biological psychiatry. Neuropsychiatry |
| مصطلحات موضوعية: | alzheimer's disease, insulin resistance, irs1, gsk3b, pkc, Neurosciences. Biological psychiatry. Neuropsychiatry, RC321-571 |
| الوصف: | Introduction. The risk of Alzheimers disease (AD) is increased with cerebral insulin resistance, which may be caused by the impaired function of the cerebrovascular system, and may also have a direct effect on -amyloid aggregation and Tau protein phosphorylation. Aim. To study the molecular expression of insulin signal transduction components (IRS1, GSK3B and PKC) in the brain cells in an experimental model of AD. Materials and methods. Experiments were conducted on 4-month-old C57BL/6 and B6.129S6-Nlrp3tm1Bhk/JJ male mice (NLRP3 knockout mice) with 5 animals in each group. AD was modelled in the experimental group of mice by administering -amyloid; mice in the control group received sham surgery. IRS1, GSK3B and PKC expression in the amygdala was studied using immunohistochemistry methods. Results. The C57BL/6 mice with AD had reduced IRS1 expression compared with the mice who received sham surgery (0.620.13 and 0.890.17; р=0.045), while the -amyloid did not produce the same result in NLRP3 knockout mice. GSK3B expression was increased in C57BL/6 mice with AD (0.600.12) when compared with both the control group (0.200.02; p0.0001) and the NLRP3 knockout mice with AD (0.270.08; p0.0001). PKC expression in C57BL/6 mice with AD was reduced (0.520.14) when compared with the NLRP3 knockout mice with AD (0.890.18; p0.05) and the control group (0.840.12; p0.05). Conclusion. The development of Alzheimer type-neurodegeneration is accompanied by disruptions in IRS1 and GSK3B expression, which is associated with impaired signal transmission along the PKC pathway. The suppression of neuroinflammation through NLRP3inflammasome deletion has a protective effect in AD. |
| نوع الوثيقة: | article |
| وصف الملف: | electronic resource |
| اللغة: | English Russian |
| تدمد: | 2075-5473 2409-2533 |
| Relation: | https://annaly-nevrologii.com/journal/pathID/article/viewFile/617/489; https://doaj.org/toc/2075-5473; https://doaj.org/toc/2409-2533 |
| DOI: | 10.25692/ACEN.2019.4.5 |
| URL الوصول: | https://doaj.org/article/e6d9424252c74f178550323aff72d704 |
| رقم الانضمام: | edsdoj.6d9424252c74f178550323aff72d704 |
| قاعدة البيانات: | Directory of Open Access Journals |
| تدمد: | 20755473 24092533 |
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| DOI: | 10.25692/ACEN.2019.4.5 |