Alzheimer's disease is a progressive, incurable and ultimately fatal type of dementia that typically affects people later in life. It is marked by the death of neurons, which is thought to be caused by clumps of a protein called A-beta. The effects of A-beta on the brain are still being studied in order to better understand the disease.
A-Beta Identification
A-beta, also known as beta-amyloid, is a small protein fragment that is made from a larger protein known as amyloid precursor protein, or APP, the Alzheimer's Association explains. Although researchers do not know what the function of the amyloid precursor protein is, they do know that it appears to be embedded in cell membranes in the body. APP is broken down into several different protein fragments in the body, one of which is called A-beta.
Amyloid Plaques and Alzheimer's
The A-beta peptide is able to cluster together to form dense coils of protein that are referred to as amyloid, the American Health Assistance Foundation explains. These plaques accumulate throughout the body and can be seen under a microscope. It is thought that these amyloid plaques can form on neurons where they cause neuronal dysfunction and neuron death, which leads to the symptoms of Alzheimer's. This conceptualization of how Alzheimer's is developed is called the amyloid hypothesis, the Alzheimer's Association explains.
A-Beta Forms
Because A-beta is a fragment of a larger protein, it can exist in many different forms that vary based on size. The two main forms of A-beta are called A-beta40 and A-beta42, the Genetics Company explains. A-beta40 is the most common form of A-beta. A-beta42, on the other hand, forms aggregates much more easily. Patients with Alzheimer's disease typically have a greater ratio of A-beta42 to A-beta40, which suggests that Alzheimer's disease is caused by elevated amounts of the longer form of A-beta, causing amyloid plaques to form in the brain.
Evidence for Amyloid Hypothesis
Although researchers have not been able to definitively prove that the accumulation of forms of A-beta into amyloid is responsible for the development of Alzheimer's disease, there are a number of pieces of evidence that support the so-called amyloid hypothesis. First of all, genetic mutations that cause patients to produce more A-beta can lead to Alzheimer's disease, the Alzheimer's Association notes. Mice that are genetically manipulated to have these mutations also develop amyloid plaques and some of the symptoms associated with Alzheimer's disease. In addition, patients with Down's syndrome have three copies of the APP gene instead of the normal quantity of two, and they also develop amyloid plaques at an early age.
Genetic Mutations
Alzheimer's disease can be divided into inherited and non-inherited forms. Scientists do not know what triggers the disease in patients with the latter form. People with inherited forms of Alzheimer's disease, on the other hand, have specific genetic mutations. Some of these mutations, the Mayo Clinic explains, can have mutations that cause them to make more of A-beta42, which leads to the rapid development of amyloid plaques. Other patients have mutations in the A-beta protein, which cause it to aggregate more quickly and at lower concentrations. Patients with this kind of Alzheimer's disease typically get it earlier in life.
