POSSIBLE THERAPEUTIC ROLE OF &lt;I&gt;JASONIA CANDICANS&lt;/I&gt; AND &lt;I&gt;JASONIA MONTANA&lt;/I&gt; EXTRACTS IN THE REGRESSION OF ALZHEIMERâS DISEASE IN EXPERIMENTAL MODEL

Ahmed Ahmed

doi:10.3844/ajbbsp.2013.144.161

Abstract

The present article aimed to investigate the potent ial role of the ethanolic extracts of the aerial pa rts of Jasonia candicans and Jasonia montana in management of Alzheimer’s Disease (AD) in experimental model. Supplementation of drinking water AlCl 3 (0.3%) for 16 weeks induced AD in male rats with siginifcant increase in brain Acetylcholinesterase (AchE) activity, Tumour Necrosis Factor (TNF-α), Transforming Growth Factor β (TGF-β) and 8 hydroxydeoxyguanosine (8-OHdG) levels. AlCl3 supplementation produced significant decrease in Br ain insulin Like Growth Factor (IGF-1) and Derived Neurotrophic Factor (BDNF) levels as compared to the control values. Also, AlCl 3 supplementation caused significant decline in the expression levels of nuc leoporin P 62 (P 62 ) and a disintegrin and metalloproteinase 17 (ADAM 17) genes accompanied with significant elevation in the expression levels of brain cyclooxygenase (Cox-2) gene. Brain histopa thological examination of AD-induced rats showed formation of amyloid plaques in hippocampus and cerebrum. Oral administration of each of selected extract (150 mg/kg b.wt) in AD-induced rats daily f or 6 weeks resulted in significant decrease in brai n AchE activity, TNF-α, TGF-β and 8-OHdG levels. The treatment produced signific ant increase in brain IGF-1 and BDNF levels as compared to AD-induced rats. The treatment with these extracts could significantly increase the gene expression levels o f brain P 62 and ADAM17 accompanied with significant decrease in the expression levels of Cox-2 gene in the brain. Histopathological examination of brain tissue of the treated rats showed marked improvement in the morphological structure of the brain especially in the hippocampus and cerebrum areas. H igh content of terpenes, sesquiterpenes and flavonoids in the ethanolic extract of the selected plants may responsible for the anticholinesterase activity, anti-inflammatory action, antioxidant cap acity and neurotrophic effect as well as antiamyloidogenic potential of these extracts. These re sults suggest that these extracts may effectively ameliorate the inflammation and neurodegeneration characterizing AD. Thus, these extracts may have a therapeutic application in the treatment of Alzheim er’s disease.

Highlights

Alzheimer’s Disease (AD) is a heterogeneous progressive age-related neurodegenerative disease of the brain that affects memory, thought, reasoning and language
The data in Table (1) represented the effect of Jasonia candicans and Jasonia montana extracts on brain cholinesterase activity and Tumor Necrosis Factor-α (TNF-α) level in AD model induced in male rats by receiving AlCl3 in drinking water for 4 months
In comparison with AD-induced group treated with rivastigmine, treatment of AD-induced group with Jasonia candicans or Jasonia montana extract caused significant decrease (p

Summary

Introduction

Alzheimer’s Disease (AD) is a heterogeneous progressive age-related neurodegenerative disease of the brain that affects memory, thought, reasoning and language It is characterized by a progressive memory decline as well as serious cognitive disability due to the progressive dysfunction and death of nerve cells that are responsible for the storage and processing of information (Takeda et al, 2008). Such mechanisms include Aβ toxicity, cholinergic dysfunction, tau protein hyperphosphorylation, oxidative damage, synaptic dysfunction and inflammation secondary to senile plaques (Bernhardi, 2007). Oxidative modifications of both nuclear DNA and mitochondrial DNA have been proposed as one biochemical change that could lead to the neuropathology, neuronal dysfunction and death in AD (Polidori et al, 2007). There are strong indications that oxidative stress occurs prior to the onset of symptoms in AD and oxidative damage is found mainly in the vulnerable regions of the brain affected by this disease (Casadesus et al, 2007)

Results

Discussion

Conclusion