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Alzheimer’s Disease

When they no longer know your name

Karen Miller | 5/18/2015, 6 a.m.
Alzheimer’s disease, the most common form of dementia, is a progressive, degenerative disease that robs victims of memory, reasoning, thinking ...
Reisa A. Sperling, M.D., M.MSc., Director, Center for Alzheimer Research and Treatment, Brigham and Women’s Hospital, Professor of Neurology, Harvard Medical School Photo courtesy Brigham and Women’s Hospital

Time’s impact on the body is pretty obvious. The hair thins and turns white. Lines and wrinkles invade the skin. We can even lose an inch or two in height.

There are some changes, however, we cannot see. The brain is aging as well. The memory gets a little fuzzy. You walk into a room and can’t for the life of you figure out why. These are mild changes, however, and cause little harm — just annoyance.

Yet, something more sinister can lurk undetected — all due to errant proteins. Tangles of a protein called tau (rhymes with “wow”) accumulate in nerve cells in the brain that are called neurons. Clumps of another protein, called amyloid plaques, build up between nerve cells and interrupt communication.

These are not good changes. The tangles strangle the cells causing their eventual demise, while plaque prevents communication between the neurons. Unfortunately, it’s that communication that allows memory, reasoning, emotion, movement and even breathing. Scientists now believe that the amyloid plaque is the major culprit here and drives the production of the tangles in the cells.

Alzheimer’s is a progressive disease that results in nerve cell death and tissue loss throughout the brain. Plaques and tangles, which are the precursors to AD, are depicted in the blue-shaded areas. As the disease progresses, the brain shrinks, which eventually impacts most of its functions.

Alzheimer’s is a progressive disease that results in nerve cell death and tissue loss throughout the brain. Plaques and tangles, which are the precursors to AD, are depicted in the blue-shaded areas. As the disease progresses, the brain shrinks, which eventually impacts most of its functions.

“It is normal for neurons to produce these proteins,” said Dr. Reisa Sperling, the director of the Center for Alzheimer Research and Treatment at Brigham and Women’s Hospital. “But it is not normal for them to accumulate.” Few are spared. “Almost everyone over the age of 65 has some tau in the hippocampus (the part of the brain that controls memory and learning),” she explained. “Roughly 30 percent have the amyloid plaque in the cortex.” The cortex controls complex functions like problem solving, emotions and comprehension.

This buildup of proteins begins earlier in life, but may go undetected for decades. Some people experience these changes to some extent with no side effects. However, in Alzheimer’s disease, the most common form of dementia, these proteins take over and wreak havoc. And their impact is very noticeable.

AD is a progressive, degenerative disease that robs victims of memory, reasoning, thinking and communication and eventually their life. It is the sixth leading cause of death in this country.

It is estimated that 5.4 million people have AD. In a recent study published in the journal Neurology, however, researchers concluded that the number is considerably higher. That’s because while the immediate causes of death are often attributed to pneumonia or other conditions, the fatalities are precipitated by AD.

Undoubtedly, the number will continue to climb. By 2030 — just 15 years away — one-fifth of the U.S. population will be 65 years or older, according to the U.S. Census Bureau. And age is the largest risk factor for AD.

The impact of AD on the economy is staggering. According to the National Institutes of Health, in 2010 the cost to treat AD was roughly $215 billion. As a point of comparison, in that same year the cost to treat cancer was $77 billion, noted the NIH.

The cause of AD is not exactly known. It is likely due to a combination of genetic, environmental and life-style factors. A gene, familiarly known as APOE — APOE-4, to be exact — is thought to play a role in the development of AD. Sperling is quick to point out that the inheritance of APOE-4 merely increases the risk, and is not a definitive cause of AD. In addition, some people lacking that form of the gene can still develop AD.