Alzheimer's, Dementia & Mental Health
Keeping Brain Active Protects Against Alzheimer’s But May Be Too Late for Seniors
Study finds beta-amyloid causing protein not as common in those enjoying mental activities
Jan. 24, 2012 – A new study confirms the long-held belief that keeping the brain active as we age
provides protection from the development of Alzheimer’s disease, but it also pin-points the biological cause. For older people, however, it is not all
good news, since the most protection appears to develop before people become senior citizens.
Brain scans revealed to the researchers from the University of California, Berkeley that people with no symptoms of
Alzheimer’s who engaged in cognitively stimulating activities throughout their lives had fewer deposits of beta-amyloid, a destructive protein
that is the hallmark of the disease.
While previous research has suggested that engaging in mentally stimulating activities – such as reading, writing and
playing games – may help stave off Alzheimer’s later in life, this new study identifies the biological target at play. This discovery could
guide future research into effective prevention strategies.
“These findings point to a new way of thinking about how cognitive engagement throughout life affects the brain,” said
study principal investigator Dr. William Jagust, a professor with joint appointments at UC Berkeley’s Helen Wills Neuroscience Institute, the
School of Public Health and Lawrence Berkeley National Laboratory.
“Rather than simply providing resistance to Alzheimer’s, brain-stimulating activities may affect a primary pathological
process in the disease. This suggests that cognitive therapies could have significant disease-modifying treatment benefits if applied early
enough, before symptoms appear.”
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PET scans reveal amyloid plaques, which appear as warm colors such
as red and orange. The middle scan is from a person with no symptoms of cognitive problems, but with evident levels of amyloid plaque
in the brain. (Images by Susan Landau and William Jagust) |
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A molecular model of amyloid protein fibrils. Formed when mis-folded
proteins self-assemble into fibrous sheet structures, they are found in the brains of sufferers of Alzheimer's disease. |
An estimated 5.4 million Americans live with Alzheimer’s disease, but the numbers are growing as baby boomers age.
Between 2000 and 2008, deaths from Alzheimer’s increased 66 percent, making it the sixth-leading killer in the country.
There is currently no cure, but a draft of the first-ever National Alzheimer’s Plan, released this week, revealed that
the U.S. government is aiming for effective Alzheimer’s treatments by 2025.
The new study, published Monday, Jan. 23, in the Archives of Neurology, puts the spotlight on amyloid – protein fibers
folded into tangled plaques that accumulate in the brain. Beta-amyloid is considered the top suspect in the pathology of Alzheimer’s disease,
so finding a way to reduce its development has become a major new direction of research.
The researchers note that the buildup of amyloid can also be influenced by genes and aging – one-third of people age 60
and over have some amyloid deposits in their brain – but how much reading and writing one does is under each individual’s control.
“This is the first time cognitive activity level has been related to amyloid buildup in the brain,” said study lead
author Susan Landau, research scientist at the Helen Wills Neuroscience Institute and the Berkeley Lab.
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Alzheimer's, Dementia & Mental Health |
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“Amyloid probably starts accumulating many years before symptoms appear. So it’s possible that by the time you have
symptoms of Alzheimer’s, like memory problems, there is little that can be done to stop disease progression. The time for intervention may be
much sooner, which is why we’re trying to identify whether lifestyle factors might be related to the earliest possible changes.”
The researchers asked 65 healthy, cognitively normal adults aged 60 and over (average age was 76) to rate how frequently
they participated in such mentally engaging activities as going to the library, reading books or newspapers, and writing letters or email. The
questions focused on various points in life from age 6 to the present.
The participants took part in extensive neuropsychological testing to assess memory and other cognitive functions, and
received positron emission tomography (PET) scans at the Berkeley Lab using a new tracer called Pittsburgh Compound B that was developed to
visualize amyloid. The results of the brain scans of healthy older individuals with various levels of lifetime cognitive activity were
compared with those of 10 patients diagnosed with Alzheimer’s disease and 11 healthy people in their 20s.
The researchers found a significant association between higher levels of cognitive activity over a lifetime and lower
levels of beta-amyloid in the PET scans. They analyzed the impact of other factors such as memory function, physical activity, self-rated
memory ability, level of education and gender, and found that lifelong cognitive engagement was independently linked to amyloid deposition.
Notably, the researchers did not find a strong connection between amyloid deposition and levels of current cognitive
activity alone.
“What our data suggests is that a whole lifetime of engaging in these activities has a bigger effect than being
cognitively active just in older age,” said Landau.
The researchers are careful to point out that the study does not negate the benefits of kicking up brain activity in
later years.
“There is no downside to cognitive activity. It can only be beneficial, even if for reasons other than reducing amyloid
in the brain, including social stimulation and empowerment,” said Jagust. “And actually, cognitive activity late in life may well turn out to
be beneficial for reducing amyloid. We just haven’t found that connection yet.”
Author Affiliations: Helen Wills Neuroscience Institute (Drs Landau, Mormino, Rabinovici, Oh, and Jagust and Mr
Marks) and School of Public Health (Dr Jagust), University of California, Berkeley, and Life Sciences Division, Lawrence Berkeley National
Laboratory, Berkeley, California (Drs Landau, Rabinovici, O’Neil, and Jagust); Memory and Aging Center and Department of Neurology, University
of California, San Francisco (Dr Rabinovici); and Rush Alzheimer's Disease Center, Rush University Medical Center, Chicago, Illinois (Dr
Wilson).
The National Institutes of Health and the Alzheimer’s Association helped support this research.
Original story by by
Sarah Yang, Media Relations, UC Berkeley
