الفهرس 
INTRODUCTIONOnly 14 pages are availabe for public view
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Abstract
Alzheimer’s disease (AD) is degenerative brain condition and the most widespread reason of dementia. It accounts for nearly 60-80% of all dementia cases. AD is associated with cognitive decline and memory loss. The number of people diagnosed with AD is projected to be 13.8 million by the year 2060. The AD brain exhibits severe neurodegenerative changes such as synapsis and neurons loss, beta amyloid plaques deposition.
Aluminum is a strong neurotoxin in both humans and animals. Several studies suggest that Aluminum is involved in the rise of oxidative stress as well as inflammatory markers, which disrupts intraneuronal metal homeostasis and affects long-term potentiation and transport in axons. Previous research has noticed a clear connection between Aluminum deposition in the brain and the advancement of symptoms like Alzheimer such as of phosphorylated tau aggregation, which comprises of neurofibrillary tangles and the deposition of Amyloid beta plaques.
Despite the significant and chronic impacts of Alzheimer’s disease, present medications cannot achieve sufficient therapeutic benefits or halt the disease progression. Nowadays, only five medications are approved by the FDA for Alzheimer’s’ treatment. So, there is a keen interest in the development of natural medications for treating cognitive decline during AD.
Vanillic acid, a well-known flavonoid, is prevalent in a variety of plants, fruits and nuts. Vanillic acid has been discovered to possess antimicrobial, antioxidant and anti-inflammatory properties, in addition to reducing the activity of snake venom. The antioxidant effect of Vanillic
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acid includes scavenging of free radicals and increasing antioxidative status. Vanillic acid has been studied for its neuroprotective impact in cerebral ischemia and neurodegenerative illnesses such as Parkinson’s disease and Alzheimer’s disease.
The present study was carried out on 40 male Sprague Dawley rats 6 weeks old with an average body weight of 150-200 g. Rats were randomly divided into five groups: each group containing 8 rats.
I- Negative control group (Control): Rats were intraperitoneally injected with saline for 4 weeks.
II- Alzheimer’s induced group (AD): Rats were intraperitoneally injected with AlCl3 (50 mg/kg body weight) for 4 weeks (Jyoti et al., 2007).
III-Alzheimer’s induced group treated with Vanillic acid (AD+VA): Rats were intraperitoneally treated with (50 mg/kg vanillic acid) + (50 mg/kg) AlCl3 for 4 weeks (Singh et al., 2015).
IV- Alzheimer’s induced group pretreated with Vanillic acid (VA+AD): Rats were intraperitoneally treated with vanillic acid one week before injection with AlCl3.
V- Vanillic acid group (VA): Rats were intraperitoneally treated with vanillic acid (50 mg/kg body weight) for 4 weeks.
After the completion of behavioral studies, the rats were sacrificed, and hippocampus tissue was removed from each animal and divided into two parts. One part was immersed in 10% neutral buffered formalin for histopathological stain (H&E), histochemical stain (crystal violet), and immunohistochemical detection of BCL-2. The other part was stored at -80 C for determining the expression levels of ERK1/2 and GSK3-β genes using qRT-PCR.
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The results of present study are emphasized as the following,