Published in the journal Nature Neuroscience, and the results demonstrate the potential value of 43 A as a biomarker for the diagnosis of AD and suggest a potential role of new approaches to prevent AD-causing amyloidosis, promising hope for AD patients around the world.An irreversible, progressive brain disease that affect millions of people around the world, Alzheimer’s disease is devastating to its victims, depriving them of their memory and cognitive abilities, and ultimately their lives. Even after decades of research, however, the causes of Alzheimer’s remains elusive. Two features of the brain, abnormal clumps (senile plaques) and tangled bundles of fibers (neurofibrillary tangles) are known to characterize AD, but there is little consensus on the relationship between these characteristics and root causes of the disease.
A hypothesis that has attracted widespread support suggests that AD is caused by the accumulation of senile plaques, and in particular their main constituent, amyloid peptides (A). Two major forms of A, A 40 and A 42 were associated with genetic mutations that cause early-onset AD, and have received considerable attention and research. The role of most species, however, that also exist in the brains of Alzheimer’s patients, has not yet been fully studied.
Researchers at the RIKEN Brain Science Institute (BSI) and their colleagues have highlighted the role of a little studied in promoting amyloid of Alzheimer’s disease (AD). Their surprising results show that the peptide is more abundant, more neurotoxic and has a greater propensity to aggregate amyloidogenic agents studied in previous research, suggesting a potential role in new approaches to prevent AD-causing amyloidosis.
In their work, researchers have focused on the A 43, a peptide amyloid in the brain, as is often the patient as a 42, but relatively little is known. To investigate the role of the peptide in AD, have generated mice with a mutation resulting in overproduction of A 43 and used a very sensitive to the distinction between the concentrations of A 40, A 42 and A 43.
Their results show that a surprising 43 is most abundant in the brain of AD patients over 40 years, and more neurotoxic A 42. A 43 is also the highest propensity to aggregate and accelerates amyloid pathology. Moreover, unlike the other two of a kind that exist in the human and mouse brain at birth, 43 levels appear to increase with age, consistent with the model of AD onset.