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Prevalence and Causes of Alzheimer's Disease

Carrie Steckl, Ph.D., edited by Natalie Staats Reiss, Ph.D.

research graphAccording to Alzheimer's Disease International, in 2015, it is estimated 46.8 million people worldwide have Dementia and that Alzheimer's Disease accounts for 70-75% of these cases.  This number of those living with Dementia will almost double every 20 years, reaching 74.7 million in 2030 and 131.5 million in 2050.  There are over 9.9 million new cases of dementia each year worldwide, implying one new case every 3.2 seconds.

The risk of developing AD increases dramatically with age; almost 50% of individuals over 85 are coping with this disorder.

Causes of Alzheimer's Disease

Despite the increasing interest in research focused on the causes of Alzheimer's Disease, scientists are still uncertain about the true reason (or reasons) why individuals develop the illness. Most likely, there is no one single factor that we can pinpoint as a culprit. Most experts think that several factors are working together to ultimately determine whether someone goes on to develop AD.

Before we explain the brain changes that occur with Alzheimer's Disease, it's important to understand what happens to people's brains as they age. Remember, we said before that AD is a disease process rather than normal aging. Therefore, it is important to continue our "compare/contrast" between normal aging and Alzheimer's to further illustrate what happens to people's brains when they have the disease.

The Aging Brain

Three major processes happen to people's brains as they get older. First, some neurons (nerve cells in the brain and spinal cord) shrink. Second, plaques and tangles develop. Third, free radical damage increases. These factors combine to cause a slowing of reaction time and some minor impairment in a person's ability to remember and to learn new things. These changes are part of the normal aging process.

Plaques are deposits of a protein called beta-amyloid that accumulate in the spaces between neurons in the brain. Beta-amyloid fragments break off of a larger protein called amyloid precursor protein (APP). When people are young, APP helps damaged neurons repair themselves as well as stimulating neurons to regrow after injury (if necessary). As people age, APP breaks up into beta-amyloid fragments and mixes with molecules, neurons, and other types of cells, creating clumps (plaques). These clumps can interfere with the neurons' ability to communicate with each other and perform important brain functions.

Neurofibrillary tangles are deposits of a protein called tau. Tau's job is to help make long fibers called microtubules which act as miniature scaffolds, holding the neuron in its proper shape and also helping transport nutrients within the neuron. As people age, tau stops working properly in some neurons and starts to accumulate and twist around inside the cells. As a result, the microtubules collapse, causing impaired communication between neurons, and eventually, cell death. The fiber tangles remain in the brain long after the dead neuron has been cleared away.

Free radicals are unstable molecules that are created during metabolism (when the body breaks down food into nutrients), immune system reactions (when the body is trying to fight off viruses and bacteria), and exposure to certain environmental factors (e.g., pollution, radiation, cigarette smoke). Free radicals typically attack the nearest stable molecule, causing it to become unstable itself, in turn creating another free radical, and so on (a process called oxidation). When we are young, the body is usually able to cope with free radicals by mobilizing antioxidants (nutrients that prevent oxidation such as Vitamins C and E). However, as we age, free radical damage accumulates, creating cell and tissue damage (causing wrinkles, hearing loss, etc.).