Amyloid is a protein that is expressed in many different organ systems. When amyloid gets misprocessed and accumulates, it causes neurodegeneration. One of the hallmarks of Alzheimer’s disease (AD) is the accumulation of amyloid plaques (abnormally configured proteins) between nerve cells (neurons) in the brain. Amyloid-beta (Aβ) is a small, sticky portion of the amyloid protein that contributes to plaque formation. A healthy brain is able to break down amyloid-beta and eliminate it, but in AD, Aβ forms insoluble plaques that are toxic to neurons and sometimes (not always) associated with AD-related memory loss and other changes.

Previously, amyloid accumulation could only be observed after an autopsy, but advances in neuroimaging and biomarker assessments have made it possible to measure Aβ plaque buildup over time and learn which parts of the brain are most affected.

Anti-amyloid drugs are being tested in clinical trials, with the hope of preventing the formation of Aβ plaques in the future.


Role of Amyloid-Beta

Amyloid plaque deposits have long been associated with neurodegeneration in Alzheimer’s disease (AD); however, the precise ways in which the toxic damages neurons are still being explored. 

What we know is that dense deposits of two proteins, , and tau, overtake the brains of people with Alzheimer’s disease, and the brain suffers atrophy, neuronal cell death, and damaged blood vessels, which deprives the brain of oxygen and nutrients and causes toxins to accumulate.

It seems that deposits drive all other changes in the brain that are associated with AD (including tangled deposits of tau, blood vessel deterioration, neuronal cell death, and brain atrophy).  But exactly how and why is still unclear.