Amyloid is a general term for fragments of proteins that the body produces normally but which can also form pathological aggregates. Amyloid is characterized by long, fibrous strands that are formed when beta amyloid protein aggregates.
Beta amyloid (β amyloid, Aβ) is a protein fragment cleaved from the amyloid precursor protein (APP) in the brain. In a healthy brain, these protein fragments are broken down and eliminated.
In Alzheimer’s disease (AD), where the clearance of amyloid is impaired, the amyloid fragments accumulate into small toxic aggregates called beta amyloid oligomers, which are considered the key pathogenic factor in AD, and then into insoluble plaques that are the hallmarks of the disease.
Amyloid aggregation and plaques have been associated with the pathology of more than 20 serious human diseases. With advanced age, when the clearance of beta amyloid is impaired, beta amyloid proteins aggregate and accumulate into toxic soluble beta amyloid oligomers, triggering a cascade of events leading to injury of brain cells, neurodegeneration or neuropathology, and resulting in conditions such as Alzheimer’s disease and cerebral amyloid angiopathy.