Boston - Researchers have developed innovative techniques to provide more evidence that Alzheimer’s pathology is originated in Amyloid-Beta (Abeta) oligomers in the brain, rather than the amyloid plaques, previously thought by many researchers to cause the disease. Additionally, this new research will facilitate the development of new neuroimaging agents and drugs to treat Alzheimer’s by specifically targeting oligomers.
Supported by Cure Alzheimer’s Fund (CAF), the research led by Dr. Sam Gandy, Professor in Alzheimer’s disease Research at the Mount Sinai School of Medicine and the James J. Peters VAMC, and a member of the CAF research consortium, together with Dr. Michelle Ehrlich, Professor of Pediatrics and Neurology, also at Mount Sinai, was published as an Accepted Article in the online version of the journal Annals of Neurology this month. Dr Charles Glabe, an oligomer expert and a member of the CAF research consortium, is also a co-author of the paper, as is John Steele, a Mount Sinai graduate student, who performed the key analyses of the behavioral data.
“While no one has been able to identify a definitive cause for Alzheimer’s, our research validates the recent shift in attention from Abeta plaques to Abeta oligomers, which are floating clumps of the Abeta protein,” said Gandy. “This will help to better understand the causes of this devastating disease and even open up new doors for more effective treatments.”
Dr. Gandy’s research, using the CAF funding, studied mice that developed Abeta oligomers and memory impairment but no plaques; and, in parallel, a related line of mice that formed both oligomers and plaques. Tests showed that mice with the complete absence of plaques were just
as impaired by the disease as those with both plaques and oligomers, confirming the impact of oligomers on Alzheimer’s pathology.
“These mice may also enable the development of a new generation of neuroimaging agents that will allow us to visualize brain oligomer burden during the course of the patient’s life,” Gandy said. “The mice may also aid in the development of drugs that could detoxify the oligomers in the brain.”
Development of a new neuroimaging agent that could monitor changes in Abeta oligomer presence would be a major improvement over the pioneering Pittsburgh compound B (PiB) technique, which shows plaques in the brain but cannot recognize oligomers. Innovative neuroimaging agents that will allow researchers to visualize brain oligomer accumulation in tandem with careful clinical observations while patients are living could lead to breakthroughs in managing, slowing, stopping or even preventing Alzheimer’s. This is especially important in light of research reported in March showing that seventy weeks of infusion of the Abeta immunotherapeutic Bapineuzumab® cleared away 25% of the PiB-detectable Abeta plaque, yet no clinical benefit was evident.
“As always, we are very proud of the results yielded by Dr. Gandy’s ability to look past conventional beliefs and explore new directions in Alzheimer’s research,” said Tim Armour, president and CEO of Cure Alzheimer’s Fund. “His work offers hope to the millions of Americans and their families affected by the disease every day. We can’t get to the cure without understanding the cause of this devastating disease.”
About Cure Alzheimer's Fund
Cure Alzheimer's Fund™ is a 501c3 public charity whose mission is to fund research with the highest probability of slowing, stopping or reversing Alzheimer's disease. Cure Alzheimer’s Fund is characterized by a venture approachto philanthropy, which targets funding to specific research objectives. All expenses and overhead is paid for by its founders and all contributions go directly to research. The Foundation has no financial or intellectual property
interest in the research funded, and will make known the results of all funded research as soon as possible. Cure Alzheimer’s Fund is a national organization with offices in Boston and Pittsburgh. For more information, visit www.curealzfund.org.
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