Affiliations 

  • 1 Medical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Elgomhourya street, Mansoura, 36551, Egypt. toxicsalama@hotmail.com
  • 2 Medical Experimental Research Center (MERC), Faculty of Medicine, Mansoura University, Elgomhourya street, Mansoura, 36551, Egypt
  • 3 Toxicology Department, Faculty of Medicine, Mansoura University, Mansoura, Egypt
  • 4 Internal Medicine Department, Faculty of Veterinary Medicine, Mansoura University, Mansoura, Egypt
  • 5 Urology and Nephrology Center (UNC) Faculty of Medicine, Mansoura University, Mansoura, Egypt
  • 6 Department of Clinical Pharmacology, Faculty of Medicine, Menoufia University, Shebeen El-Kom, Egypt
Neurotox Res, 2019 May;35(4):987-992.
PMID: 30362086 DOI: 10.1007/s12640-018-9974-3

Abstract

Tauopathy is a pathological hallmark of many neurodegenerative diseases. It is characterized by abnormal aggregates of pathological phosphotau and somatodendritic redistribution. One suggested strategy for treating tauopathy is to stimulate autophagy, hence, getting rid of these pathological protein aggregates. One key controller of autophagy is mTOR. Since stimulation of mTOR leads to inhibition of autophagy, inhibitors of mTOR will cause stimulation of autophagy process. In this report, tauopathy was induced in mice using annonacin. Blocking of mTOR was achieved through stereotaxic injection of siRNA against mTOR. The behavioral and immunohistochemical evaluation revealed the development of tauopathy model as proven by deterioration of behavioral performance in open field test and significant tau aggregates in annonacin-treated mice. Blocking of mTOR revealed significant clearance of tau aggregates in the injected side; however, tau expression was not affected by mTOR blockage.

* Title and MeSH Headings from MEDLINE®/PubMed®, a database of the U.S. National Library of Medicine.