Alzheimers disease is the most common cause of severe memory impairment and is caused by senile plaques, neurofibrillary tangles, dystrophic neuritis, and neuronal loss. It is thought that Alzheimers disease may be due to unnecessary protein accumulation of β Amyloid. In fact, Senile plaques are dense, protein deposits composed of amyloid β peptide. The two types of senile plaques are diffuse plaques and neuritic plaques, and differ in morphology. In addition to the amyloid, the microtubule-associated Tau protein has also been in involved with Alzheimers disease and a variety of other neurodegenerative diseases. Inherited forms of Alzheimers have been linked to mutation in the APP genes or presenilins which regulate APP processing.
Because cholinergic neurons of the nucleus basalis are significantly altered during Alzheimer's progression, cholinergic agents such as choline and lecithin were hypothesized to augment the progression. However, these attempts were unsuccessful and the only clinically useful drugs used in the United States are cholinesterase inhibitors, which prolong the time before choline degradation. Although  receptor antagonists and anti-inflammatory drugs were tested in a clinical environment, more promising clinical trials are underway to targeting the Aβ with the immune system.