Amiri S, Azadmaneshb K, Dehghan Shasaltaneh M, Khoshkholgh-Sima B, Naghdi N. Protein Kinase Cε in the Platelet and Hippocampal Tissue as a Diagnostic Biological Marker in Alzheimer Disease. BCN 2019; 10 (6) :545-556
URL:
http://bcn.iums.ac.ir/article-1-1376-en.html
1- Department of Physiology and Pharmacology, Pasteur Institute of Iran, Tehran, Iran.
2- Department of Virology, Pasteur Institute of Iran, Tehran, Iran.
3- Department of Biology, Faculty of Sciences, University of Zanjan, Zanjan, Iran.
Abstract:
Introduction: Alzheimer disease (AD) is a neurodegenerative disorder characterized by the progressive loss of memory and other cognitive functions. Protein kinase Cε (PKCε) is an isoform that most effectively suppresses amyloid beta (Aβ) production and synaptic loss.
Methods: In this study, spatial learning and memory for treated rats were evaluated by the Morris water maze test. The activity (total PKC), mRNA expression, and protein level of PKCε in the platelet and hippocampal tissue were evaluated using immunosorbent assay, real-time qPCR, and western blotting analysis, respectively.
Results: The traveled distance was significantly prolonged, and escape latency significantly increased in Aβ-treated groups. PKC activity assay showed that there was a remarkable difference between the Aβ-treated and sham-operated groups on days 10 and 30 in the hippocampus and also day 30 in platelet after the injection of Aβ. A significant effect in PKC activity was observed between days 0 and 10, days 0 and 30, as well as days 5 and 30. Aβ significantly downregulated the PKCε mRNA expression in the hippocampus of rats on day 30; however, no significant difference was observed in platelet. Western blot analysis demonstrated that Aβ significantly reduced PKCε protein expression in the hippocampus of treated groups on day 30.
Conclusion: The expression level of PKCε was downregulated following the injection of Aβ in the hippocampus, but no significant difference was observed between the AD and sham groups in platelet that may be due to the low concentration of PKCε or duration of Aβ exposure in the rat brain.
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● Amyloid beta (Aβ) significantly downregulated the PKCε mRNA expression in the hippocampus of rats on day 30.
● Aβ could not significantly downregulate the PKCε mRNA expression in platelet on day 30.
● Western blot analysis demonstrated that Aβ significantly reduced PKCε protein expression in the hippocampus of treated groups on day 30.
● The expression ratio of PKCε was downregulated following the injection of Aβ in the hippocampus.
● There was no significant difference between the Alzheimer and sham groups in the platelet.
Plain Language Summary
Alzheimer disease (AD) is one of the most important neurodegenerative disorders characterized by neurofibrillary tangles and senile plaques. Protein kinase C (PKC) is a family of serine/threonine protein kinases that are involved in signal transduction in the central nervous system. Abnormalities in the levels and activities of protein kinase C isozymes have been reported in the brain and other tissues. PKC is one of the enzymes related to amyloid precursor protein. In the neurons of AD patients, the first abnormality is a defect in the PKC signal channels. The inhibition of PKC activity leads to the reduced capacity of learning and memory. In the present study, spatial learning and memory for treated rats were evaluated by the Morris Water Maze (MWM) test. Also, the activity, mRNA expression, and protein level of PKCε in the platelet and hippocampal tissue of rat brains were evaluated. According to the results, the expression of PKCε was downregulated following the injection of amyloid beta in the hippocampus, but no significant difference between the AD and sham groups were observed in platelet that may be due to the low concentration of PKCε or duration of exposure to amyloid beta in the rat brain.
Type of Study:
Original |
Subject:
Behavioral Neuroscience Received: 2018/12/3 | Accepted: 2019/02/7 | Published: 2019/11/1