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Amyloid beta peptide plays a role in Alzheimer’s and other neurological diseases. Beta-amyloid plaques form from a 42-amino acid long peptide, inhibiting brain function. Genetic inheritance of the 42AA peptide increases the risk of Alzheimer’s. Potential therapies include beta-secretase and gamma-secretase inhibitors, as well as amyloid beta antibodies.
Amyloid beta protein is a large peptide containing between 39 and 43 amino acids. This peptide chain is thought to play an important role in the development of Alzheimer’s disease. The plaques that develop in the brains of people with Alzheimer’s are composed primarily of amyloid beta peptide. This peptide may also play a role in the development of other neurological diseases such as Lewy body dementia.
Beta-amyloid plaques are formed primarily of a 42-amino acid long peptide. The most common form of the peptide has only 40 amino acids, but the 42AA peptide has a greater tendency to form plaques. Plaques form because the protein is fibrillogenic, meaning it has a tendency to clump together with other similar proteins to form fibrous structures. These structures are the plaques that progressively inhibit normal brain function in people with Alzheimer’s disease.
Research suggests that plaques cause dementia because these clumps of peptide fibers attach to neurons in the brain. Once attached, the fibers prevent neurons from receiving signals from other cells in the brain. The affected neurons cannot function or communicate with other brain cells and as a result they die.
Alzheimer’s is partially genetically inherited, a trait that is associated with a tendency to produce amyloid beta peptides that are 42 amino acids long. When an individual has a copy of the gene that produces the 42AA peptide, they have a higher risk of developing Alzheimer’s disease. A person with two copies of this gene is at high risk of developing early-onset Alzheimer’s.
Based on this knowledge of how the protein interacts to form plaques, researchers have come up with several ideas that are being explored as potential therapies to treat Alzheimer’s disease. One of them is an enzyme called beta-secretase inhibitor. This enzyme may be able to block the cleavage of the amyloid protein into the 42AA form which is most strongly associated with the development of Alzheimer’s. A related idea is a gamma-secretase enzyme, which prevents the formation of peptide 42AA at another point in the production cycle.
Another approach to treating Alzheimer’s is the development of an amyloid beta antibody that can recognize and bind to the 42AA peptide. These antibodies may be able to bind to the peptide and prevent it from forming plaques. Additionally, the antibody may help promote the destruction of the peptide, as the immune system will destroy any antibody-peptide complexes that are formed.
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