ABSTRACT
Alzheimer’s Disease (AD) is a progressive and neurodegenerative disorder of the brain characterized by loss of neurons and synapses, particularly in regions related to memory and cognition. The main neuropathological features of AD are accumulation of abnormal intracellular and extracellular proteinaceous deposits in the brain of the patients (Alois Alzheimer in 1907)—within neuronal cells, as accumulation of abnormally phosphorylated tau protein into paired helical filaments, known as neurofibrillary tangles (NFTs) (Terry, 1994) and outside cellular structures as proteinaceous aggregates in form of amyloid plaques and as amyloid in the wall of cerebral blood vessels (Masters et al., 1985; Selkoe, 1991). The sequence of pathological events leading to the observed deposits and finally to neurodegeneration is
believed to start with the abnormal processing of the amyloid precursors protein (APP), leading to the generation of Ab (Kang et al., 1987). The hypothesis states that the Ab protein triggers through formation of toxic aggregates the subsequent formation of NFTs, loss of synapses, and finally loss of neuronal function. This sequence of events is now described as the amyloid cascade (Figure 4.1).
