Jul 4, 2011 07:32 GMT  ·  By
Microscopy image of a neurofibrillary tangle, characteristic to Alzheimer's disease patients
   Microscopy image of a neurofibrillary tangle, characteristic to Alzheimer's disease patients

Scientists looking for new ways of counteracting the effects of Alzheimer's disease now have a new avenue of research to go on. A team of experts with the RIKEN Brain Science Institute (BSI) has just provided new insights into how a specific peptide influences the development of this condition.

This little-studied amyloid peptide is apparently involved very deeply with promoting the onset and development of Alzheimer's in seniors. The molecule is even more dangerous that the amyloidogenic agents that other studies covered.

Scientists focused their research on the amyloid-β (beta) peptide Aβ43. Their work uncovered that the molecule is more neurotoxic, more likely to aggregate, and more abundant than other, similar peptides or proteins researchers analyzed before.

Amyloidosis, the accumulation of proteins or peptides in clumps or tangles inside the brain, is believed to be one of the main causes of Alzheimer's. By understanding more about Aβ43, the BSI team enabled a new series of studies on the disease.

Now that experts know how the peptide operates, it may become easier to develop treatments targeting this molecule specifically. The therapy could function either by itself, or in conjunction with existing drugs. Unfortunately, the root cause of Alzheimer's remains obscured.

Senile plaques and neurofibrillary tangles are the two main features that are distinguishable in the brain of patients. This is an irreversible neurodegenerative condition, a form of dementia that reduces neural function. This leads to cognitive decline, memory loss, and other negative side-effects.

The molecules Aβ40 and Aβ42 have in the past been linked to genetic mutations that lead to the early onset of Alzheimer's disease, and have therefore received a lot of attention. Other forms of amyloid-beta peptides have been largely ignored in the process.

Aβ43 was found to be more neurotoxic than Aβ42, and more abundant than Aβ40. Interestingly, it was also found that its levels increase with age, whereas concentrations of the other two remain constant since birth. Details of the new work appear in the latest issue of the top journal Nature Neuroscience.