Print ISSN 2319-2003 | Online ISSN 2279-0780
doi: http://dx.doi.org/10.18203/2319-2003.ijbcp20150855
IJBCP International Journal of Basic & Clinical Pharmacology
www.ijbcp.com International Journal of Basic & Clinical Pharmacology | September-October 2015 | Vol 4 | Issue 5 Page 853
Research Article
Neuroprotective effect of renin angiotensin system blockers on
experimentally induced Alzheimer’s disease in rats
Wafaa A. Hewedy
1
, Wessam F. El-Hadidy
2
*
INTRODUCTION
Alzheimer’s disease (AD), the most common form of
dementia, is an insidious, progressive disorder characterized
by subtle behavioral and memory disturbances; progressing
into global cognitive impairment, memory loss, behavioral
and psychiatric disturbances, and functional impairment.
1
The greatest risk factor for the development of AD is
advancing age. However, the exact mechanisms of AD are
incompletely understood.
2
One of the key pathological features of AD is deposition of
a 40-42 amino acid peptide called amyloid-β (Aβ). Aβ is
the building brick for Aβ peptide (Aβ-P) that is deposited
in the brain as extracellular senile plaques, or within the
walls of the cerebrovasculature.
3
Development of drugs that
reduce Aβ deposition through inhibition of its production
or increased promotion of its removal is now a major
therapeutic strategy.
Much evidence points to a link between hypertension and
AD.
4
High systolic blood pressure is reported to be associated
with low brain weight, whereas a high systolic and diastolic
blood pressure are associated with increased prevalence
of the neurofbrillary tangles (NFT) in hippocampal brain
regions.
5
Although the use of antihypertensive drugs has
ABSTRACT
Background: Alzheimer’s disease (AD) is a major world-wide health problem.
Much evidence points to a link between hypertension and AD. However, the exact
effects of different antihypertensive drugs on AD need to be more assessed. The aim
was to evaluate and compare the possible effects of perindopril, and candesartan on
cognitive impairment, oxidative stress markers, and brain concentrations of amyloid
beta-peptide (Aβ-P) in a rat model of induced dementia.
Methods: Thirty-two adult male Wistar rats were distributed among 4 groups;
(1) normal controls; (2) rats with dementia induced by intracerebroventricular
administration of streptozotocin (ICV-STZ) and received no treatment; (3) ICV-STZ
rats treated orally with perindopril for 3 weeks; and (4) ICV-STZ rats treated orally
with candesartan for 3 weeks. The assessed parameters were spatial memory by
Morris Water Maze test, brain tissue level of total antioxidant capacity (TAC), reduced
glutathione (GSH), lipid peroxidation product (malondialdehyde [MDA]), and Aβ-P.
Results: Both perindopril and candesartan attenuated STZ-induced memory
impairment, caused a signifcant increase in TAC and GSH levels, reduced MDA
levels, whereas only candesartan signifcantly reduced Aβ-P levels.
Conclusions: This study reports that candesartan and perindopril can reverse the free
radical induced damages and resultant memory defects, and may suggest candesartan
as worthy drugs for prevention of Aβ-P deposition in this animal model of AD.
Keywords: Streptozotocin, Amyloid beta-peptide, Hypertension, Perindopril,
Candesartan, Oxidative stress
1
Department of Clinical
Pharmacology, Faculty
of Medicine, Alexandria
University, Alexandria, Egypt,
2
Department of
Pharmacology and
Experimental Therapeutics,
Medical Research Institute,
Alexandria University,
Alexandria, Egypt
Received: 24 August 2015
Accepted: 14 September 2015
*Correspondence to:
Wessam F. El-Hadidy,
Email: drwessamhadidy@
gmail.com
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Medip Academy. This
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