London, Jul 4 (ANI): A new research has shown that a little-studied amyloid peptide could play a greater role in promoting Alzheimer's disease (AD), suggesting a potential role in new approaches for preventing AD-causing amyloidosis.
One hypothesis that has attracted widespread support proposes that AD is caused by the buildup of the senile plaques, and in particular of their main constituent, amyloid-B peptides (AB). Two major forms of AB, AB40 and AB42, have been associated with genetic mutations causing early-onset AD, and have thus received considerable research attention.
In their current work, the researchers at the RIKEN Brain Science Institute focused on AB43, an amyloid-B peptide found just as often in patient brains as AB42, but about which relatively little is known. To study the peptide's role in AD, they generated mice with a mutation causing overproduction of AB43, and used a highly sensitive system to distinguish between concentrations of AB40, AB42 and AB43.
Their surprising results reveal that AB43 is even more abundant in the brains of AD patients than AB40, and more neurotoxic than AB42. AB43 also exhibits the highest propensity to aggregate and considerably accelerates amyloid pathology. Moreover, unlike the other two AB species, which exist in human and mouse brains at birth, AB43 levels appear to increase with age, consistent with the pattern of AD onset.
The findings thus reveal the possible value of AB43 as a biomarker for diagnosis of AD and suggest a potential role in new approaches for preventing AD-causing amyloidosis, promising hope to AD sufferers around the world.
The study has been published in the journal Nature Neuroscience. (ANI)
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