Evaluation of aβ deposits in hippocampus of ad rat model after intravenous injection of hadscs by immuno- and thioflavin s- costaining

Mina Eftekharzadeh,1,* Maryam doshmanziari,2 Marjan shariatpanahi,3 Arash sarveazad3,4 Fatemeh moradi,5

1. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran
2. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran
3. Department of Toxicology & Pharmacology, School of Pharmacy, International Campus, Iran University of Medical Sciences, Tehran, Iran
4. Colorectal Research Center, Iran University of Medical Sciences, Tehran, Iran
5. Department of Anatomy, Iran University of Medical Sciences, Tehran, Iran

Abstract


Introduction

Alzheimer,s disease (ad) is a progressive neuropsychiatry disorder that gradually deteriorates memory and behavioral functions. amyloid beta (aβ) is considered as the most toxic substances in the ad brain. aβ immunofluorecent staining distinguishes fibrillar and non-fibrillar aβ, whereas thioflavin-s (thio-s) identifies the β-pleated fibrillar amyloid form of ad. the present study was designed to evaluate aβ deposits in hippocampus of ad rat model after intravenous injection of human adipose derived stem cells (hadscs).

Methods

Twenty-four male rats were used in 4 groups; control, sham, ad rat model, and hadscs treatment group. the hadscs characterization was confirmed by flowcytometry technique. an immuno- and thioflavin s- costaining (double staining method) wasutilized for detecting aβ plaques in ad rat model following injection of hadscs.

Results

Statistical analysis revealed that administration of hadscs significantly decreased immunoreactive and thio-s positive plaques number in ad group (###pvalue< 0.001). we also found that the plaques detected by anti-beta amyloid antibody were significantly more than plaques which distinguished by thio-s in all the groups (f [3, 40] = 0.15, p =0.928). conclusion: consequently, our results showed that the hadscs had effective role in decreasing amyloid aggregation following migration to the site of injury.

Conclusion

As aβ toxicity is the major reason of neuronal death in ad, hadsc may be a promising candidate for ad therapy due to its high potential for clearance of aβ deposits.

Keywords

Alzheimer ,s disease; thioflavin; amyloid beta-protein; stem cell transplantation