LONDON, July 5 (Xinhua) -- Researchers at the Medical Research Council's Laboratory of Molecular Biology (LMB) say on Wednesday that for the first time they have succeeded in revealing the atomic structures of one of the abnormal filaments which lead to Alzheimer's disease.
They say understanding the structures of the filaments is key to the development of drugs to prevent their formation, and will help find better compounds for diagnosing and treating Alzheimer's.
The researchers, whose study is published in the journal Nature, believe the structures they have uncovered could also suggest how tau protein may form different filaments in other neurodegenerative diseases.
The team says their findings open up a whole new era in neurodegenerative diseases and should make it easier to design drugs to stop brain cells dying.
Alzheimer's, the most common of neurodegenerative diseases, is characterized by the existence of two types of abnormal "amyloid" forms of protein which form lesions in the brain.
The latest academic research paper comes almost 30 years ago since scientists at the LMB identified tau protein as an integral component of the lesions found in Alzheimer's and a range of other neurodegenerative diseases. Until now scientists have been unable to identify the atomic structure of the filaments.
Tau forms filaments inside nerve cells and amyloid-beta forms filaments outside cells. Tau lesions appear to have a stronger correlation to the loss of cognitive ability in patients with the disease.
Dr Rob Buckle, chief science officer at the MRC, which funded the research, said: "This ground-breaking work is a major contribution to our understanding of Alzheimer's disease. Nearly thirty years ago scientists at the LMB were the first to discover that tau protein plays a key role in the disease. Knowing the basic structure of these filaments in diseased tissue is vital for the development of drugs to combat their formation.
"This research opens up new possibilities to study a range of other diseases where the accumulation of abnormal protein filaments plays a role, including Parkinson's disease, motor neuron disease and prion diseases."
Fellow senior author Dr Michel Goedert, who also worked on the original research 30 years ago, said: "We have known for almost three decades that the abnormal assembly of tau protein into filaments is a defining characteristic of Alzheimer's disease.
"Until now the high-resolution structures of tau or any other disease-causing filaments from human brain tissue have remained unknown. This new work will help to develop better compounds for diagnosing and treating Alzheimer's and other diseases which involve defective tau."
