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We don't know what causes Alzheimer's disease. Risk factors include age, having a first degree relative with the disease, having had a head injury in the past, and having low levels of physical activity, hypertension, diabetes, high cholesterol or atrial fibrillation.

There are two types of Alzheimer's disease: early-onset and late-onset. Early-onset Alzheimer's disease is rare, affecting only about 5% of people with the disease. People with the early-onset form usually develop the disease between the ages of 30 and 60. Late-onset Alzheimer's disease makes up the bulk of cases, and affects people after the age of 60.

Although we are still teasing out the details, we know that genetic factors play some role in the disease as people with an affected first degree relative are at a higher risk of developing the disease. The only genetic risk factor that we know of so far for developing late-onset Alzheimer's disease is a particular form of the ApoE protein gene (called the ApoE e4 allele).

Early-onset Alzheimer's disease also has genetic links. A particular type, called familial Alzheimer's disease, is caused by one of three known genetic mutations. Children of affected people have a 50% chance of inheriting their parent's genetic mutation; those that do will almost certainly develop the disease. The mutations we know of so far are in the genes for amyloid precursor protein (APP), presenilin 1 (PS1) or presenilin 2 (PS2). These mutations cause abnormal proteins to form in the brain, which leads to an increased amount of a protein called beta amyloid.

All people with Alzheimer's disease - both early and late-onset - have been found to have an abnormal build-up of this protein in their brains, which clusters between the brain cells in what we call plaques. Another protein called tau forms what we call tangles inside the brain cells.

While researchers have shown that the amount of these proteins in the brain corresponds with the severity of symptoms in Alzheimer's disease, we don't yet understand the role of beta amyloid and tau in the disease process.

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