Adipose-Derived Mesenchymal Stem Cells Partially Compensating the Neurodegenerative Signs at The Behavioral, Physiological, and Molecular Levels in AD Rat Model | ||
| Egyptian Academic Journal of Biological Sciences, D. Histology & Histochemistry | ||
| Article 8, Volume 13, Issue 2, December 2021, Pages 101-118 PDF (1.15 M) | ||
| Document Type: Original Article | ||
| DOI: 10.21608/eajbsd.2021.200376 | ||
| Authors | ||
| Emad M Elzayat1; Asmaa Husein2; Yasmine Elbeltagy2; Fatma Mohamed2; Mohamed Hosney1 | ||
| 1Zoology Department, Faculty of Science, Cairo University | ||
| 2Biotechnology/Biomolecular Chemistry Program, Faculty of Science, Cairo University, Giza, Egypt Giza, 12613, Egypt | ||
| Abstract | ||
| Alzheimer's disease (AD) is the most common form of dementia. Due to the multifaceted nature of AD pathology and limited understanding of its etiology, AD is difficult to be treated with currently available pharmaceuticals. Recent studies suggest that transplantation of mesenchymal stem cells might have therapeutic potential on several neurodegenerative disorders. In addition, it can ameliorate neuropathological deficits and physiological disorders in AD. The current study aims to evaluate the potential therapeutic effect of adipose-derived mesenchymal stem cells (ADMSCs) in AD rat model after the induction with AlCl3. After the induction phase, labeled ADMSCs have been injected intravenously. Open-field behavioral tests were conducted, serum β-amyloid levels, cholinesterase activity, and brain antioxidant status were evaluated. Besides, the expression of apoptotic and necrotic markers was quantified via RT-qPCR in brain tissues. Histopathological alterations in the brain were examined as well. Signs of dementia as manifested by behavioral tests have been recorded in AD rats, accumulation of β-amyloid in blood, reduced serum cholinesterase activity and both apoptotic and necrotic induction in brain tissues had been recorded at the end of the induction phase. All these alterations have been partially/fully compensated by the administration of ADMSCs, which proved their ability to penetrate the blood-brain barrier and home in the brain tissues. The molecular mechanism underlying the therapeutic effect of ADMSCs seems to be correlated with the reduction of neurodegeneration by upregulating the anti-apoptotic marker (Bcl2) and downregulating the pro-apoptotic markers (p53 and Bax) and necrotic factor (Tnfa) simultaneously. | ||
| Keywords | ||
| Alzheimer's disease; Adipose-derived mesenchymal stem cells; β-amyloid; Acetyl cholinesterase; and Apoptosis | ||
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