Alzheimer’s disease begins at the synapse, the space where neurons connect. The biggest bad guy in this disease is a sticky protein called beta-amyloid. Either too much is made or not enough is cleared away, and as beta-amyloid accumulates, it creates a gooey clog in the synapse, preventing the neurons that meet there from communicating. As a result, the information those neurons carry can’t be transmitted or retrieved. The beta-amyloid “goo” prevents these two neurons from “talking” to each other. We notice this molecular event because we forget something.
When too much beta-amyloid causes the synapse to fail, we begin to see the symptoms of Alzheimer’s. There are many risk factors that can contribute to having too much beta-amyloid. What are these risk factors?
First, let’s imagine a seesaw-style scale and the risk factors, which each vary in weight, are being piled on one arm of the scale. When that arm hits the floor, we have Alzheimer’s.
The biggest risk factor for developing Alzheimer’s is age. For reasons we still don’t entirely understand, as we get older, we accumulate more beta-amyloid. The chances of being diagnosed with Alzheimer’s increase steadily as we age. Right now, the risk of Alzheimer’s doubles every year after the age of 65. About half of people who are 85 and older have Alzheimer’s.
Another risk factor is genetics. There is a rare form of Alzheimer’s called Familial Alzheimer’s, which always begins well before the age of 65 (typically in the 40s and 50s) and runs in families, that is autosomal dominant. This means that a single genetic mutation causes the disease. Picture the seesaw scale again. Genetic mutation is the only risk factor on the scale, and the arm is sitting on the floor.