Scientists at the University of Western Ontario used magnetic resonance imaging to examine the brains of 504 people across North America who had enrolled in the Alzheimer's disease neuroimaging initiative — at the onset of the study and six months later.
They found that when ventricles enlarge, the surrounding brain tissue dies. The increase in size occurs during mild cognitive impairment and continues to do so as Alzheimer's sets in and progresses. Ventricles are one of a system of four communicating cavities within the brain and are filled with cerebrospinal fluid.
The study also found that patients who had Alzheimer's at the beginning of the study had 60 per cent more rapid expansion of ventricles compared to people with mild cognitive impairment.
"These findings mean that, in the future, by using magnetic resonance imaging [MRI] to measure changes in brain ventricle size, we may be able to provide earlier and more definitive diagnosis," said Robert Bartha, lead author of the study, in a release.
"In addition, as new treatments for Alzheimer's are developed, the measurement of brain ventricle changes can also be used to quickly determine the effectiveness of the treatment."
Alzheimer's has traditionally been difficult to diagnose, as amyloid plaques, the sticky coverings that form outside neurons, are usually discovered only during an autopsy.
The study is published online Friday in the journal Brain.
Only in June last researchers found that the brains of people with the memory-robbing form of dementia were cluttered with such plaques.
There long has been a question whether this is a cause of the disease or a side effect. Also involved are tangles of a protein called tau; some scientists suspect this is the cause.
In mice experiments, forms of soluble beta-amyloid containing different numbers of molecules, as well as insoluble cores of the brain plaque, were injected into the brains of rats. There was no detectable effect from the insoluble plaque or the soluble one-molecule or three-molecule forms, Dr. Ganesh Shankar and Dr. Dennis Selkoe of Harvard Medical School had reported.
But the two-molecule form of soluble beta-amyloid produced characteristics of Alzheimer's in the rats, they said. The beta-amyloid seemed to affect synapses, the connections between cells that are essential for communication between them.
Dr. Marcelle Morrison-Bogorad, director of the division of neuroscience at the National Institute on Aging,said the findings may help explain the discovery of plaque in the brains of people who do not develop dementia. For some time, doctors have wondered why they find some brains in autopsy that are heavily coated with beta-amyloid, but the person did not have Alzheimer's.
The answer may lie in the two types of beta-amyloid that did not cause symptoms.
Now, the question is why one has the damaging effect and not others.
"A lot of work needs to be done," Morrison-Bogorad said. "Nature keeps sending us down paths that look straight at the beginning, but there are a lot of curves before we get to the end."