Alzheimer\'s disease (AD),the most common type of dementia,has been identified as a protein misfolding disease with the accumulation of abnormally folded amyloid-β (Aβ) protein and hyperphosphorylated tau protein in the brain [1,2].Aβ is known to play a crucial role in the pathogenesis of AD.Deposition of Aβ protein in the brain parenchyma causing senile plaques is the obligatory event in AD pathogenesis.Aβ protein is also deposited in the media and adventitia of small and midsized cerebral arteries leading to cerebral amyloid angiopathy (CAA),which is also present in the large majority of AD patents.