The following descriptions and links are from the Alzheimer’s Disease Education and Referral Center, or ADEAR. ADEAR is an Alzheimer’s disease education and information service provided by the National Institute on Aging/National Institute of Health. Contact ADEAR toll-free at 1-800-438-4380 or by email, adear@nia.nih.gov.
Alzheimer’s disease is an irreversible, progressive brain disorder that slowly destroys memory and thinking skills and, eventually, the ability to carry out the simplest tasks. In most people with Alzheimer’s, symptoms first appear in their mid-60s. Alzheimer’s disease is the most common cause of dementia among older adults.
Scientists continue to unravel the complex brain changes involved in the onset and progression of Alzheimer’s disease. It seems likely that damage to the brain starts a decade or more before memory and other cognitive problems become evident. During this preclinical stage of Alzheimer’s disease, people seem to be symptom-free, but toxic changes are taking place in the brain. Abnormal deposits of proteins form amyloid plaques and tau tangles throughout the brain, and once-healthy neurons stop functioning, lose connections with other neurons, and die.
Mild cognitive impairment (MCI) is a condition in which people have more memory or other thinking problems than normal for their age, but their symptoms do not interfere with their everyday lives. Older people with MCI are at greater risk for developing Alzheimer’s, but not all of them do. Some may even go back to normal cognition. Studies are underway to learn why some people with MCI progress to Alzheimer’s and others do not.
Many, but not all, people with Down syndrome develop Alzheimer’s disease when they get older. People with Down syndrome are born with an extra copy of chromosome 21, which carries the APP gene. This gene produces a specific protein called amyloid precursor protein (APP). Too much APP protein leads to a buildup of protein clumps called beta-amyloid plaques in the brain. By age 40, almost all people with Down syndrome have these plaques, along with other protein deposits, called tau tangles, which cause problems with how brain cells function and increase the risk of developing Alzheimer’s dementia. However, not all people with these brain plaques will develop the symptoms of Alzheimer’s. Estimates suggest that 50 percent or more of people with Down syndrome will develop dementia due to Alzheimer’s disease as they age, many now into their 70s.
Dementia is the loss of cognitive functioning—thinking, remembering, and reasoning—and behavioral abilities to such an extent that it interferes with a person’s daily life and activities. Dementia ranges in severity from the mildest stage, when it is just beginning to affect a person’s functioning, to the most severe stage, when the person must depend completely on others for basic activities of daily living.
Vascular dementia, considered the second most common form of dementia after Alzheimer’s disease, results from injuries to the vessels supplying blood to the brain, often after a stroke or series of strokes. Vascular dementia and vascular cognitive impairment arise as a result of risk factors that similarly increase the risk for cerebrovascular disease (stroke), including atrial fibrillation, hypertension, diabetes, and high cholesterol. The symptoms of vascular dementia can be similar to those of Alzheimer’s, and both conditions can occur at the same time. Symptoms of vascular dementia can begin suddenly and worsen or improve during one’s lifetime.
Lewy body dementia (LBD) is another common brain disorder in older people. LBD is caused by abnormal deposits of a protein called alpha-synuclein in the brain. These deposits, called Lewy bodies, can lead to problems with thinking, movement, behavior, and mood. For example, symptoms may include changes in alertness and attention, hallucinations, tremor, muscle stiffness, sleep problems, and memory loss.
Frontotemporal disorders are a form of dementia caused by a family of brain diseases known as frontotemporal lobar degeneration (FTLD). These disorders are the result of damage to neurons (nerve cells) in parts of the brain called the frontal and temporal lobes. As neurons die in the frontal and temporal regions, these lobes atrophy, or shrink. Gradually, this damage causes difficulties in thinking and behaviors controlled by these parts of the brain. Many possible symptoms can result. They include strange behaviors, emotional problems, trouble communicating, or difficulty with walking and other basic movements.
Autopsy studies looking at the brains of people who had dementia suggest that a majority of those age 80 and older probably had “mixed dementia,” caused by processes related to both Alzheimer’s disease and vascular disease. In fact, some studies indicate that mixed vascular-degenerative dementia is the most common cause of dementia in the elderly. In a person with mixed dementia, it may not be clear exactly how many of a person’s symptoms are due to Alzheimer’s or another type of dementia.
Posterior Cortical Atrophy, or PCA, is most commonly an atypical clinical presentation of Alzheimer’s disease. People with PCA often come to the clinic because they are having trouble interpreting information they see with their eyes (known as “visual processing impairment”), rather than with symptoms of memory loss. Because memory loss is the most common presenting symptom of Alzheimer’s disease, PCA is referred to as “atypical Alzheimer’s disease."