Toxic Proteins Linked to Brain Diseases

Amyloid fibrils are thread-like chains of protein that self-assemble as a result of a genetic flaw or changes in body chemistry brought about by aging.  When this occurs, short fibers are formed which become sticky and attract copies of themselves, forming an endless chain. These chains spontaneously break, creating more filament ends to which more proteins attach.  In the context of neurodegenerative diseases, it is thought that these short, broken pieces may cause harm.  Cait MacPhee, from the University of Edinburgh (United Kingdom), and colleagues  have observed that  when protein levels are low, lots of short protein threads are formed. But when protein levels are high, this spontaneous breakage stops and most protein filaments remain long.  Compared with harmful short protein fibers, long fibers do not appear to be damaging in the case of neurodegenerative diseases. Researchers therefore believe that high levels of the protein – which lead to these longer chains – may actually be protective.  Writing that: “We provide evidence for a structural transition that occurs at a critical fibril mass concentration … above which fragmentation of fibrils is suppressed,” the study authors hope that their research sheds light on neurodegenerative diseases, and leads to the development of biometerials, such as cell scaffolds, which may be used for tissue engineering for therapeutic purposes.