Margaret Gatz
|
Understanding Alzheimer's
By Katherine Yungmee Kim
Suppose you enter a room, an entirely dark space save for a dim lamp
that allows you to see several objects. When the light is turned off,
you have a picture in your mind of what was in the room—courtesy of
your iconic memory.
Associate Professor of Psychology Zhong-Lin Lu studies cognitive
deficiencies in observers at-risk for Alzheimer’s disease. With a team
of researchers, he has just completed a study that shows at-risk
patients have a faster decaying iconic memory than normal subjects. If
a college student can retain an image for 400 milliseconds, and a
normal older subject 270 milliseconds, an at-risk participant can only
hold the image for 50 milliseconds.
“The dominant view is that Alzheimer’s disease starts from higher
levels of cognition and gradually goes to the sensory cortex,” Lu
explains. “We are saying that we also find signs of Alzheimer’s in
early cortices.”Scientists have yet to determine the cause of
Alzheimer’s disease. What is known is that nerve cells malfunction and
die, though why is uncertain. Alzheimer’s is the number one disorder in
a family of dementias, afflicting four-and-a-half million Americans.
Primarily a specialist in perception, perceptual learning, attention
and brain imaging, Lu says this is his first study on Alzheimer’s. But
he joins two stalwarts in the psychology department in examining the
etiology of this debilitating brain disease.
Controlled Genetics
Psychology Professor Margaret Gatz determined that cognitive
stimulation plays an important role in positive aging. In a study of
143 pairs of Swedish twins who were discordant for dementia, low
education was shown to be a possible factor in developing Alzheimer’s
disease. The sibling not exhibiting signs of dementia was described as
“having read more books” and “being less likely to get lost.” Gatz
refers to the demented twin as “less intellectually engaged.”
As we age, our “cognitive reserve”—our brain’s cognitive functions,
such as learning and problem solving— is assaulted. While chemicals,
injuries and stress have proven to be risk factors, it may also be
possible to bolster cognitive reserve through cognitive stimulation and
good nutritional habits during one’s earlier years.
The Real Culprit
An unmistakable characteristic of Alzheimer’s is plaque deposits that
form lesions in the brain. This plaque, found to appear in the presence
of amyloid beta molecules, has been targeted as the culprit behind
early dementia and has been the subject of research for the past two
decades. But some healthy patients show the same brain lesions without
showing any signs of dementia. In 2001, Caleb Finch, University
Professor, ARCO/William F. Kieschnick Chair in the Neurobiology of
Aging, and professor of gerontology, biological sciences and
psychology, pinpointed a different, soluble form of amyloid beta called
ADDL that can spread throughout the brain in Alzheimer’s-affected
areas. Immobilizing the proper suspect molecule is a goal in
determining a successful treatment.
The Continuum
Alzheimer’s strikes ten percent of Americans 65 years and older . The rate increases with age: nearly half over 85 are affected.
Gatz calls the triumvirate of Finch, Lu and Gatz “a continuum” in the
psychology department. “We’re all needed,” she says, “to give older
people the whole story.”
|
|
|
