Alzheimer's disease (AD) is a disabling neurodegenerative disorder typical for elderly. AD is characterized by dementia that typically begins with subtle failures of memory and slowly becomes more rigorous and, eventually, completely incapacitating. Other common symptoms include confusion, poor judgment, language disturbances, agitation, withdrawal, and hallucinations. The average clinical duration of AD is eight to ten years. The earliest neurofibrillary changes that are part of the pathology of AD usually occur in medial temporal lobe structures, interrupting the neural network critical for episodic memory function. Thus affecting the ability to learn and consolidate new information. AD cause deterioration in the structure and organization of semantic memory. Deficits in executive functions responsible for the mental manipulation of information, problem solving, and cue-directed behavior occur early in the course of AD. Patients with AD also often exhibit deficits in visuospatial abilities. .
The genetic heritability of Alzheimer's disease, based on reviews of twin and family studies, range from 50% to 80%. Approximately 25% of AD is familial (two or more family members have AD). Earlier age of disease's onset (< 60 years) is explained by mutations in one of three genes; amyloid precursor protein (APP) on chromosome 21, Presenilin 1(PSEN1) (which is the most common gene to effect early onset) on chromosome 14, and Presenilin 2 (PSEN2) on chromosome 1. Pathological mutations in these genes are responsible for an autosomal dominant trait. These mutations affect the production of small protein called Aβ42 which in turn may cause the one of the two neuropathologic hallmarks of this disease; accumulation of extracellular amyloid beta (Aβ) deposits. The second neuropathologic characteristic of the disease is intracellular neurofibrillary tangles of hyperphosphorylated tau protein.