Researchers reveal how the disease progresses in the brain, shedding light on the genetic changes that make the disease a precursor to dementia
Alzheimer’s is a progressive condition, one that rapidly reduces the functions of the brain, but researchers have uncovered a way of measuring this in the real world.
Experts from the University of Wisconsin have published a new study in Nature Neuroscience that suggests the beta-amyloid “plaques” that accumulate in the brain and gradually turn Alzheimer’s into dementia may be different between patients with the disease and those that have not developed symptoms.
They looked at 26 cognitively normal people with Alzheimer’s and 25 cognitively normal people with no signs of the disease, and compared how well each person performed on a series of tests assessing memory, language and attention and novel tasks – testing the amount of information they could recall.
What is Alzheimer’s? – a brief guide Read more
Using the tests, they found that patients with Alzheimer’s tended to perform less well on some kinds of tasks. The findings add new insight into the progression of the disease and may help researchers design drugs that target that progression.
“This is really the first study that directly shows the degradation of cognition across time in Alzheimer’s disease,” says Dr Bruce Law, senior author of the study, also from the Wisconsin Alzheimer’s Disease Research Center. “This is a mechanism that Alzheimer’s causes; it’s an early mode, it’s reversible.”
Previous studies have shed light on the progression of Alzheimer’s in the brain, including one from the University of Wisconsin that identified areas of the brain affected in people with the disease. But it was not clear how this damage would progress from the initial deposits of beta-amyloid in the brain, to more serious problems. This new study provides that explanation.
“If you have a brain disease, particularly this one, that becomes Alzheimer’s, as it progresses, it changes from functional areas of the brain to areas that don’t really have to do with cognition,” says Law.
In people with Alzheimer’s, the hippocampus, part of the brain that plays a role in memory, shrinks and weakens, which Law explains may be a result of the loss of memory and the reorganisation of the brain.
As the disease progresses, the brain changes and changes more quickly, with the frontal cortex, the part of the brain associated with decision-making, critical skills like speech and judgement, becoming impaired. This stage is called the “crystallisation” period.
“That’s where you have the most dramatic degeneration of the brain,” he says.
At this stage, his team found that the association between disease-causing gene mutations and changes in the symptoms for each person was different, and that people with the specific mutations that cause Alzheimer’s tend to have a lower-than-normal risk of developing dementia. The individual genetic differences all likely originate from mutations in a single gene.
This points to one way that Alzheimer’s might be preventing progression in some people. The cause for this abnormality, however, might be the knowledge that a genetic variation makes a person more likely to develop dementia, Law adds.
Alzheimer’s research is currently at a crossroads, with the findings from the latest study fuelling speculation about what might lead to the disease.
“There’s tremendous advances in understanding how this disease works, that’s allowed us to make these discoveries,” says lead author, Dr Beth Grant, adding that recent breakthroughs are providing “incredible insight into the progression of the disease and its progression to dementia”.