(RxWiki News) There is no cure for Alzheimer's disease, and watching a loved one’s mental health degrade is an experience that no one should endure. Thankfully new research may lead to advancements in Alzeimer’s treatment.
A key distinctive sign of Alzheimer’s disease is the change in behavior of a protein called ‘tau.’ This protein is essential to neuron health and to the proper functioning of the brain.
Until recently this change has been a mystery but new antibody will allow for much deeper analysis of the tau protein.
"Ask your doctor about treating the symptoms of Alzheimer’s."
The study was led by Rakez Kayed, Ph.D., from the University of Texas Medical Branch at Galveston.
In a normal brain, the tau protein exists as an individual. However, in a brain of someone with Alzheimer’s, the tau protein forms twisted structures called ‘neurofibrillary tangles.’ Kayed discovered a new intermediate structure that is even more damaging than the tangles.
"What we discovered is that there are smaller structures that form before the neurofibrillary tangles, and they are much more toxic than the big structures, and we established that they were toxic in real human brains, which is important to developing an effective therapy," said Kayed.
The researchers developed a new antibody, called T22, that only bonds with these intermediate structures, called tau oligomers. This allowed them to analyze the prevalence of the structures in healthy brains and those with Alzheimer’s.
The team found that tau oligomer levels were as much as four times higher than in a healthy brain of the same age.
"One thing that's remarkable about this research is that before we developed this antibody, people couldn't even see tau oligomers in the brain," Kayed said. "With T22, we were able to thoroughly characterize them, and also study them in human brain cells."
The study was published in the FASEB Journal on Feb. 3rd, 2012, and funded by the Cullen Family Trust for Health Care, the Alzheimer's Drug Discovery Foundation, and the George and Cynthia Mitchell Center for Neurodegenerative Diseases.