ABSTRACT
Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by focal accumulation of specific proteins that have been modified by biochemical transformation of peptides normally present in the brain. Extracellularly deposited amyloid plaques are composed of fragments of a 40-42 amino acid protein, amyloid-β (Aβ),1-4 which is formed by the abnormal cleavage of amyloid precursor protein (APP). Intracellularly developed flame-shaped tangles are made up of hyperphosphorylated and abnormal conformational forms of the naturally present tau protein.5 Although the pathomechanism of these histological changes is not entirely known, it is believed that the deposition of these abnormal proteins leads to general neuronal loss characterized particularly by a cholinergic lesion that is responsible for the majority of the clinical symptoms of AD.
