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Hippocmapal Protein Kinase Mζ Overexpression Effect on Cognitive Performance in a Rat Model of Alzheimer’s Disease

Amini, Niloufar | 2018

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  1. Type of Document: M.Sc. Thesis
  2. Language: Farsi
  3. Document No: 51546 (06)
  4. University: Sharif University of Technology
  5. Department: Chemical and Petroleum Engineering
  6. Advisor(s): Roosta Azad, Reza; Gholamipour Badie, Hamid
  7. Abstract:
  8. Alzheimer’s disease (AD) is a neurodegenerative disease which results in synaptic depression and complete destruction in neurons in the final stages. Many pathogenesis has so far been attributed to AD but the most commonly explained pathomechanism is based on the amyloid cascade theory which results in formation of amyloid beta plaques outside and hyper phosphorylated neurofibrillary tangles of tau protein inside the neurons. One of the most well-known symptoms of AD is the disability to learn and form new memories and transform them into long term memory. The most commonly studied mechanism in memory formation, is the “long term potentiation”. Although many mechanisms and molecules are discovered to participate in LTP induction, there has known only one molecule to be necessary and sufficient for maintaining the LTP, an atypical brain particular isoform of protein kinase C, named PKMζ. The effect of this enzyme on Alzheimer’s disease has not established yet. In this study, we have examined the PKMζ overexpression effect on the amyloidopathy in CA1 region in the hippocampus of a rat model of Alzheimer’s disease. Our results show that PKMζ has overcome to improve the cognitive performance of the treated group and their performance has become more likely to the performance of the control group, and this could hopefully be an expectance of treatment aim of the disease
  9. Keywords:
  10. Alzheimer ; Beta-Amyloid Protein ; Long-term Memory ; Long Term Potentiation ; Hippocampus ; Performance Improvement

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