Based on the results of tests gauging spatial learning and memory, these mice were found to be impaired by Alzheimer's-like symptoms.
Next the researchers inserted a gene that would cause the mice to develop both oligomers and plaques.
Similar to the oligomer-only rodents, these mice "were still memory impaired, but no more memory impaired for having plaques superimposed on their oligomers," Gandy said.
Another result further strengthened the notion that oligomers were the prime cause of Alzheimer's in the mice.
"We tested the mice and they lost memory function, and when they died, we measured the oligomers in their brains," Gandy said. "Lo and behold, the degree of memory loss was proportional to the oligomer level," he said.
Gandy noted that PET scans are not able to detect oligomers in the human brain, but they do see amyloid plaques. This could help explain why recent trials of the experimental Alzheimer's drug bapineuzumab showed a reduction in plaques, but no improvement in patients' cognitive function, Gandy said.
Bapineuzumab is targeted to amyloid plaques. Whether the drug also affected the oligomers is not known, Gandy said, because the PET scans could not see them. "We don't even know whether bapineuzumab 'sees' them," he said.
The new study could help change the focus of ongoing research. "Our new 'oligomer only' mice may enable the development of imaging agents and drugs that lower oligomer levels without having plaques around to muddy the picture," Gandy said.
Researchers have long been trying to figure out the stages that lead up to plaques and tangles, Carrillo noted. "We [now] know that plaques and tangles are really the end stage of this disease," she said.
Oligomers are "toxic clumps" that could be the cause of Alzheimer's disease, Carrillo said. This study confirms for the first time that these toxic clumps are a cause of memory problems, she sai
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