(Medical Xpress) -- For the past five years, volunteers from the City of Berkeley and surrounding areas have come to Lawrence Berkeley National Laboratory to participate in an ongoing study thats changing what scientists know about Alzheimers disease.
The volunteers, most over the age of 70, undergo what can best be described as a brain checkup. Theyre asked to solve puzzles and memorize lists of words. Magnetic resonance imaging (MRI) scans image the structure of their brains in exquisite detail. Functional MRI scans allow scientists to watch portions of their brains light up as they form memories. And Positron emission tomography (PET) scans measure any accumulation of beta-amyloid, a destructive protein thats a hallmark of Alzheimers.
The goal of the Berkeley Aging Cohort Study is to reveal how our brains change as we age. The scientists also compare their findings with brain scans of Alzheimers patients.
Theyve noticed something oddand perhaps a little hopeful. Some volunteers have the same level of beta-amyloid deposition as an Azheimers patient. Yet they show no signs of the disease.
Why is this? How can two people, the same age and with the same signs of the disease, take such different paths?
It turns out that Alzheimers is more complicated than we thought, says William Jagust, a faculty senior scientist in the Berkeley Labss Life Sciences Division who also has appointments at UC Berkeleys School of Public Health and the Helen Wills Neuroscience Institute.
Jagust heads a team that conducts the cohort study, which so far includes about 80 volunteers, with more to come. Their research has put them at the forefront of a more nuanced take on Alzheimers.
Until recently, we thought the more amyloid accumulation in the brain, the greater the chance of developing the disease says Jagust. But we now believe that amyloid unleashes a chain of events that may or may not cause Alzheimers.
Its well known that many normal, older people have some beta-amyloid deposits in their brain. Its also likely true that people with beta-amyloid have a greater risk of cognitive decline and Alzheimers.
But the picture gets cloudy from there. Jagusts group has found structural and functional changes in the brains of healthy people that are associated with beta-amyloid. Some of these changes may be a prelude to Alzheimers.
And some changes may be signs that a person is actually resisting this path.
In a recent study, Jagust and colleagues asked people to commit pictures to memory while they watched their brain activity with functional MRI. Normal people with beta-amyloid deposition showed morenot lessactivity than people without beta-amyloid. One possible interpretation for this heightened activity is that it enables memory formation despite the presence of beta-amyloid. Their brains are working harder.
Were beginning to detect changes that may help people ward off cognitive decline and possibly Alzheimers, says Jagust.
Jagusts group is pursuing other questions: Is the cognitive decline associated with beta-amyloid deposition linked to the rate of deposition? Or is it more closely associated with changes in brain function that occur after beta-amyloid has done its damage?
Or perhaps cognitive decline is most closely associated with changes in brain structure. In another study, Jagusts team found that the more beta-amyloid plaque in a persons brain, the more a person is likely to have a smaller hippocampus, which is the part of the brain that forms new memories. They also found that someone with this damage is more likely to have impaired memory.
This research will help scientists determine how this constellation of eventsbeta-amyloid deposition, changes in brain function, hippocampus atrophycontributes to Alzheimers.
The search for the earliest signs of the disease has gained importance in recent years as pharmaceutical companies work to develop drug therapies that are designed to block the deposition of beta-amyloid.
There is a strong belief that Alzheimers must be treated very early, before symptoms appear, in order to be effective, says Jagust. We know that amyloid leads to negative consequences in the brain. We now need to determine how to stop these effects before they happen.