This is the first time anyone has successfully recapitulated Abeta and tau pathology in a single 3D human neural cell culture system.
Boston (PRWEB) October 13, 2014
In what is being hailed by scientists in the Alzheimer's research community as a game changing research finding, the Cure Alzheimer's Fund today confirmed that a new study release in the journal Nature demonstrates, for the first time, precisely how the early hallmark of Alzheimer's disease -- Beta-Amyloid, which forms into plaques -- stimulates the creation of the later hallmark: Tau tangles. Further, it identifies a key enzyme in this process.
This breakthrough simultaneously boosts Alzheimer's research in two vital ways; First, it gives researchers final confirmation of the "Amyloid Hypothesis," a longtime theory about how the disease develops that has been in some dispute for many years.
Second, it provides a promising new therapeutic target. “Here we show for the first time that beta-amyloid deposition by human neurons is sufficient to lead to tangles," said lead investigator Rudy Tanzi, PhD, Director of the Genetics and Aging Research Unit at Massachusetts General Hospital and Chairman of Cure Alzheimer’s Fund’s Research Consortium. "If you block the amyloid deposition, you block tangles from forming downstream."
The research by Tanzi and colleagues Drs. Doo Kim and Se Hoon Choi was conducted through the innovative development of new technology: use of human Alzheimer’s neurons derived from non-embryonic stem cells grown in a dish. "We call this system 'Alzheimer's-in-a-Dish'," Tanzi said. "This is the first time anyone has successfully recapitulated Abeta and tau pathology in a single 3D human neural cell culture system."