Protein Plaques Don't Cause Alzheimer's Disease
Protein Plaques Don't Cause Alzheimer's Disease
Nov. 27, 2001 -- By now, most of us are familiar with the "tangles and plaques" of Alzheimer's. These infamous beta-amyloid protein blobs are a tell-tale sign of the disease, but it's been unclear whether they are a cause or merely a side effect. Now, research shows that mice with plenty of plaque-causing protein will develop all the symptoms of Alzheimer's, whether or not they ever develop plaques.
When it comes to Alzheimer's disease, says Steve Snyder, PhD, "It's true that much of what we've known over the last 90 years has been focused on the plaques and tangles." He's program director, etiology of Alzheimer's disease, at the National Institute on Aging."The current thinking is that the plaques aren't so bad after all -- that it isn't the plaque, per se, but a component of the plaque that is the culprit," he tells WebMD.
In this latest series of experiments, an international research team led by Milla Koistinaho of the Academy of Sciences of the Czech Republic, looked at strains of mice engineered to develop the protein building blocks of beta-amyloid plaques -- in the amount normally present in Alzheimer's patients -- but not the plaques themselves.
The genetically-engineered mice began showing Alzheimer's-like signs of difficulty with learning and memory by the time they were three months old. And the problems grew steadily worse with age, even though the animals never developed beta-amyloid plaques.
The researchers report their results suggest plaque formation is not a necessary condition for memory impairment, but instead, the symptoms of Alzheimer's disease may be caused by an overabundance of, or glitch in, the building-block proteins.
"The mice with the mutation show cognitive changes; they don't behave like normal mice. And yet, there isn't a lot of plaque in these animals. So what's going on? The work suggests there's more to it than meets the eye, quite literally," says Snyder.
"It isn't the plaque," he tells WebMD. "The researchers suspect it's the smaller building blocks, but it isn't clear that that's absolutely true." Snyder says there just isn't enough data to know for certain. Even so, these latest findings support those of other reputable experiments and should encourage continued investigation into an alternate source for the devastating symptoms of Alzheimer's disease.
When it comes to Alzheimer's disease, says Steve Snyder, PhD, "It's true that much of what we've known over the last 90 years has been focused on the plaques and tangles." He's program director, etiology of Alzheimer's disease, at the National Institute on Aging."The current thinking is that the plaques aren't so bad after all -- that it isn't the plaque, per se, but a component of the plaque that is the culprit," he tells WebMD.
In this latest series of experiments, an international research team led by Milla Koistinaho of the Academy of Sciences of the Czech Republic, looked at strains of mice engineered to develop the protein building blocks of beta-amyloid plaques -- in the amount normally present in Alzheimer's patients -- but not the plaques themselves.
The genetically-engineered mice began showing Alzheimer's-like signs of difficulty with learning and memory by the time they were three months old. And the problems grew steadily worse with age, even though the animals never developed beta-amyloid plaques.
The researchers report their results suggest plaque formation is not a necessary condition for memory impairment, but instead, the symptoms of Alzheimer's disease may be caused by an overabundance of, or glitch in, the building-block proteins.
"The mice with the mutation show cognitive changes; they don't behave like normal mice. And yet, there isn't a lot of plaque in these animals. So what's going on? The work suggests there's more to it than meets the eye, quite literally," says Snyder.
"It isn't the plaque," he tells WebMD. "The researchers suspect it's the smaller building blocks, but it isn't clear that that's absolutely true." Snyder says there just isn't enough data to know for certain. Even so, these latest findings support those of other reputable experiments and should encourage continued investigation into an alternate source for the devastating symptoms of Alzheimer's disease.
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