New mechanism behind Alzheimer's onset identified
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Sporadic Alzheimer's disease accounts for 99% of all Alzheimer's cases, and involves the development of toxic peptide deposits in the brain. These peptide deposits cause the neuronal networks to be destroyed, leading to disorientation, memory loss, changes in behavior and death.
Although studies of Alzheimer's in animal models typically use mice with mutated human genes, the new study - conducted by researchers at the University of Oslo in Norway - used a new mouse model for the more common sporadic form of Alzheimer's.
To create this new mouse model, the function was removed from two genes in the brain that are used to excrete and digest toxic Alzheimer's peptide beta-amyloid. The researchers say this new "transgene-free" mouse model allows studies to be conducted without "artificial overexpression" of inherited Alzheimer's disease genes.
Although it has previously been assumed that overproduction of toxic peptides causes the onset and first clinical signs of Alzheimer's, the new study finds that the responsible mechanism is decreased removal of toxic peptides, rather than overproduction.
Although studies of Alzheimer's in animal models typically use mice with mutated human genes, the new study - conducted by researchers at the University of Oslo in Norway - used a new mouse model for the more common sporadic form of Alzheimer's.
To create this new mouse model, the function was removed from two genes in the brain that are used to excrete and digest toxic Alzheimer's peptide beta-amyloid. The researchers say this new "transgene-free" mouse model allows studies to be conducted without "artificial overexpression" of inherited Alzheimer's disease genes.
Although it has previously been assumed that overproduction of toxic peptides causes the onset and first clinical signs of Alzheimer's, the new study finds that the responsible mechanism is decreased removal of toxic peptides, rather than overproduction.
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