ABSTRACT
Alzheimer’s disease (AD) is characterized by degeneration and death of cerebral cortex neurons and is the major cause of dementia. Individuals, who are 65 years or older, have high risk of developing this neurodegenerative disease. Progressive loss of cognitive functions occurs in this disease. Over 90% of AD is acquired and only about 5-10% is inherited from parents. This disease is the fth leading cause of death among people aged 65 years or older. Despite extensive research on the causes of AD, it has not been possible to reduce the incidence or the rate of progression of AD. During the last few decades, several biochemical and genetic defects that contribute to degeneration and death of neurons have been identied in AD. They include: (a) increased oxidative stress, (b) mitochondrial dysfunction, (c) chronic inammation, (d) Aβ1-42 peptides generated from the cleavage of amyloid precursor protein (APP), (e) proteasome inhibition, (f) high cholesterol levels, and (g) heritable mutations in APP, presenilin-1, and presenilin-2 genes.
