Alzheimer’s disease is the most common cause of both senile and pre-senile dementia but its cause is unknown. Occasional cases are familial. The disease is characterized pathologically by the presence of neurofibrillary tangles and Alzheimer’s plaques (neuritic plaques with amyloid cores) in the brain, which in advance cases is small, with cortical atrophy and widened cerebral sulci. There is a reduced activity of cerebral choline acetyle transferase in Alzheimer’s disease, and recent studies have shown degeneration of a cholinergic pathway projecting from the subcortical nucleus basalis of Meynart to the cerebral cortex.

This is a disease characterized by irreversible, progressive and gradual loss of memory and thinking skills due to destruction of brain cells, eventually the victim can not perform the known daily activities and depends on others. This mostly occurs after 60 years, though early onset Alzheimer can occur at 30, 40 or 50 years. Alzheimer’s disease is named after Dr. Alois Alzheimer, a German psychiatrist. In 1906, Dr. Alzheimer noticed changes in the brain tissue of a woman who had died of an unusual mental illness. Her symptoms included memory loss, language problems, and unpredictable behaviour. After she died, he examined her brain and found many abnormal clumps (now called amyloidal plaques) and tangled bundles of fibres (now called neurofibrillary tangles). Plaques and tangles in the brain are two of the main features of Alzheimer’s disease.   

It is not known exactly what causes this process to begin, but people with Alzheimer's disease have been found to have abnormal amounts of protein (amyloid plaques) and fibres (tau tangles) in the brain.