Scientists Stumble Across New Alzheimer's Plaque

Scientists Stumble Across New Alzheimer's Plaque -

A protein misbehaved brain that has escaped the notice of over 0 years has emerged unexpectedly as a major cause of disease can Alzheimer. The unidentified protein form a previously unknown variety of Alzheimer's lesion that appears to be just as common as the well-known senile plaques and neurofibrillary tangles. The discovery, published in the July issue of American Journal of Pathology , could lead to new ways to diagnose and treat disease dreaded depleting memory, which hits 5% of people over 65 years of

the brains of Alzheimer's patients have been known to house at least two microscopic defects from German neurologist Alois Alzheimer first described in 107. senile plaques are composed primarily of a protein called amyloid and neurofibrillary tangles are manufactured from one tau called which freezes in masses of paired helical filaments.

To study how tau goes awry, Marie Luise Schmidt, working in the laboratory of the University of Pennsylvania School of Medicine neurobiologists John Trojanowski and Virginia Lee, created a set of antibodies that bind to different tau sections. But many of the antibodies, particularly one called AMY 117, do not work quite as expected. They bind to tau protein at all, but instead sought plates

intuition "researchers was that the tau antigen used to produce the antibodies were contaminated with proteins from senile plaques. But when Schmidt stained autopsied brain sections using both AMY 117 and an antibody to amyloid, she was surprised to find that the two types of antibodies gravitated to two different sets of plates - one of which had never been glimpsed, apparently because it is resistant to conventional staining techniques. "Their existence could not have been suspected without these new antibodies," says Trojanowski. The team found plaques in the brains of 32 AD they examined AMY binding; the plates were usually close, but do not overlap, senile plaques

The discovery means that Alzheimer's researchers now have a whole new set of disease mechanisms to explore -. and new challenges to overcome. "It could be that if you sweep plaques and tangles senile and still have these AMY plates, you will get rid of two-thirds of the symptoms," said Trojanowski, who is currently in the process of purifying the protein AMY connection with the objective to locate and clone the gene. "This opens new perspectives for us," admits neuroscientist Zaven Khachaturian, director of the Ronald and Nancy Reagan Association of Research Institute of Alzheimer's in Chicago. "It can give us new diagnostic tools, new ideas about the causes of disease, and new targets for treatment. "

Tweet