Alzheimer's Disease and Beta Amyloid
The peptide beta amyloid is a major component of the extracellular plaques that are one of the two hallmarks of Alzheimer’s disease (AD).beta amyloid protein Beta amyloid is thought to be deposited in these extracellular plaques along with the tangles of the neurofibrillary protein tau. The formation of these tangles and plaques is thought to cause the loss of neurons in the brain and the symptoms of dementia. The peptide is produced by the cleavage of the larger precursor protein amyloid precursor protein, or APP, by the enzymes beta- and gamma-secretase. These two enzymes are currently the focus of most efforts to develop a drug that will prevent their cleavage and reduce the production of peptide beta amyloid.

The human APP gene provides instructions for making a large protein that is found in many tissues and organs including the central nervous system (CNS).beta amyloid protein The protein helps regulate cell-to-cell interaction and may function as both a membrane receptor and a signaling protein. During early development, APP is involved in the migration of cells and nerves to form the brain. Mutations in the APP gene that lead to AD cause it to be cleaved more rapidly and produce more peptide beta amyloid.

In the brain, APP is cleaved by beta- and gamma-secretase to release the peptides amyloid-beta (A-beta) and A-beta 1-42.beta amyloid protein A-beta can bind to itself and other molecules to form oligomers that aggregate into the senile plaques that are characteristic of AD. In a normal brain, A-beta is degraded and eliminated by the immune system.

The aggregation of peptide beta amyloid in the CNS is the primary characteristic of AD and is a major cause of the loss of neurons and synapses observed in the disease.beta amyloid protein It is also thought to disrupt neuron-to-neuron communication at the synapse. Several drugs that either remove beta-amyloid or interfere with its production from APP have been developed and are in clinical trials. These treatments may help to delay the onset of the symptoms of dementia. These approaches include preventing the cleavage of APP by targeting the beta- and gamma-secretase enzymes or preventing its aggregation. The aggregation of A-beta is also believed to contribute to the degradation of other proteins and to the oxidative stress that is seen in AD patients.