الفهرس 
IntroductionOnly 14 pages are availabe for public view
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Abstract
Alzheimer’s disease (AD) was discovered by German psychiatrist and neuropathologist Alois Alzheimer in 1906 (Ramirez-Bermudez 2012). The term Alzheimer’s disease (AD) was used firstly by Kraepelin in 1910 based on the clinical and pathological description of Alzheimer’s original cases (Armstrong 2013). It accounts for nearly 60-80% of all dementia cases, overwhelmingly more than other dementias, such as Lewy body dementia, vascular dementia and frontotemporal dementia. There are more than 36 million people worldwide suffering greatly from AD until 2010 (Rafii and Aisen 2015). According to Alzheimer’s Association report (2010) one person in every eight people age 65 and older suffers from AD, and by the year 2050, a person will develop AD every 33 seconds (Alzheimer’s Association 2010).At the neuropathological level, there are two histopathological hallmarks of AD include deposition of extracellular β-amyloid plaques and intracellular neurofibrillary tangles (NFT) composed of aggregates of hyperphosphorylated tau protein (Cárdenas et al. 2012). Several hypotheses have been put forward on the basis of the numerous causative factors to explain this multifactorial disorder (Kumar et al. 2015). Such as (1) acceleration of aging, (2) degeneration of anatomical pathways, including the cholinergic pathway, (3) a metabolic disorder resulting from mitochondrial dysfunction, (4) environmental factors such as exposure to aluminum, head injury, and malnutrition, (5) genetic factors including, mutations of amyloid precursor protein (APP) and presenilin (PSEN) genes, and allelic variation in apolipoprotein E (Apo E), (6) tau protein (Armstrong 2013).