Alzheimer’s Trade-Off for Mentally Active Seniors

Stimulation delays cognitive decline, but disease advances quickly once it starts

September 2, 2010 RSS Feed Print

By Bruce Bower, Science News

Mental exercise lets seniors outrun Alzheimer’s disease—for a while. Then the race takes a tragic turn for the sharp-minded, a new study finds, as declines in memory and other thinking skills kick into high gear.

After age 65, regular participation in mentally stimulating activities, including doing crossword puzzles and reading, delays intellectual decay caused by Alzheimer’s disease, say neuropsychologist Robert Wilson of Rush University Medical Center in Chicago and his colleagues. But when this debilitating condition finally breaks through the defenses of a mentally fortified brain, it rapidly makes up for lost time, the scientists report in a paper published online September 1 in Neurology.

“The benefit of delaying initial signs of cognitive decline by keeping mentally active may come at the cost of more rapid dementia progression later on,” Wilson says.

His team also found that mental stimulation slows cognitive declines typically experienced by seniors with healthy brains but offers no protection against the onset of memory and thinking problems that fall short of Alzheimer’s disease.

Several recent studies have pointed to a delayed but sharp drop in thinking skills among mentally active people who develop Alzheimer’s disease, remarks neuropsychologist Yaakov Stern of Columbia University College of Physicians and Surgeons in New York City. Unlike the new report, though, those studies did not compare mentally active adults who developed Alzheimer’s disease with those who remained healthy or lost some mental function.

“This cognitive trade-off is a good one if a mentally active person suffers with clinical symptoms of Alzheimer’s disease for a shorter period of time,” Stern says.

Adults who learn to succeed at various intellectual challenges develop cognitive resources needed to cope with early stages of brain disease, Stern hypothesizes.

Wilson’s team studied 1,157 healthy Chicago residents with a range of incomes and ethnic backgrounds, ages 65 and older. To gauge mental activity levels, participants reported how often they watched television, visited museums, played cards or other games, listened to radio and read newspapers, magazines and books.

Each person underwent two or three evaluations over six years. At the end of the period the researchers identified 148 individuals with Alzheimer’s disease and 395 volunteers with milder forms of brain disease.

Those who initially reported high overall rates of mental activity displayed pronounced cognitive declines after being diagnosed with Alzheimer’s disease, Wilson says. Mentally inactive adults who developed the brain disease suffered moderate cognitive hits.

Given individual differences in the severity and onset of Alzheimer’s disease, these findings are consistent with a delay of months or years in cognitive decline among mentally active adults, followed by plummeting mental faculties, the researchers hold.

Biostatistician Charles Hall of Albert Einstein College of Medicine in New York City led a 2009 study that found a similar pattern of cognitive decline among elderly Bronx residents who stayed mentally active. Wilson’s analysis of a larger, more diverse sample of adults supports current thinking that mental training programs (SN: 5/24/08, p. 7) and other cognitive interventions work best if initiated before symptoms of Alzheimer’s disease appear, Hall says.

Researchers are now looking for biological markers of Alzheimer’s disease (SN: 2/18/06, p. 102), which may affect as many as 5.1 million U.S. adults.

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Tags:
Alzheimer's disease,
senior health,
memory,
mental health

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The Alzheimers Reading Room has clear, concise, usable news, research, insight and advice for the entire Alzheimers community.

The website focuses on those suffering from Alzheimers disease and Dementia, Alzheimers caregivers, and the art of Alzheimers caregiving.

100 Million people have been touched by Alzheimer's disease, and 35 million are worried about Alzheimer's.

http://www.alzheimersreadingroom.com/2010/02/about-alzheimers-reading-room.html

Bob DeMarco of FL 11:19PM September 02, 2010

Alzheimers is related to blood sugar even in NON Diabetics. The filmmaker who has been reversing diabetes WITHOUT medications has shown proof of the Alzheimers link to diabetes...even in non diabetics

just google SPIRIT HAPPY DIET

Mary of CA 9:14PM September 02, 2010

Do not drink the water in that town!

Scientists who study the genetics of Alzheimer’s distinguish between “familial Alzheimer’s disease,” which runs in families, and “sporadic Alzheimer’s disease”, where no obvious inheritance pattern is seen. True familial Alzheimer’s disease accounts for less than 5% of Alzheimer’s cases. Sporadic Alzheimer’s is much more common.

Familial Alzheimer’s Disease

All Familial Alzheimer’s disease known so far has an early onset, and as many as 50 percent of the cases are now known to be caused by defects in three genes located on three different chromosomes, the structures inside cells that house the genetic code. Some families have mutations in a gene called amyloid precurser protein (APP), which causes an abnormal form of the amyloid protein to be produced. Other families have mutations in a gene called presenilin 1, which causes an abnormal presenilin 1 protein to be produced. Still others have mutations in a very similar gene called presenilin 2, which causes an abnormal presenilin 2 protein to be produced.

Even if one of these mutations is present in only one of the two copies of a gene inherited from a person’s parents, the person will inevitably develop that form of early-onset Alzheimer’s (this is called autosomal dominant inheritance). However, the total known number of these cases is small (between 100 and 200 worldwide), and there is as yet no evidence that any of these mutations play a major role in the more common, sporadic or non-familial form of late-onset Alzheimer’s. Scientists are working to reveal the normal function of APP and presenilins and to determine how mutations of these genes cause the onset of familial Alzheimer’s disease.

Marcus of IL 5:19PM September 02, 2010

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