In the tradition of scientific breakthroughs often derive from very unexpected place , an antibiotic in use since 1989 has shown potential for breaking the Hz that leads to Alzheimer ’s disease . Given the failure rate of initially promising drug against Alzheimer ’s , there is a long fashion to go on this one . Nevertheless , the fact the drug in interrogative sentence involves a fundamentally different approach to block up the neurological disease than most of those tried so far could mean it ’s just what we postulate .
The symptoms of Alzheimer ’s are surd to recite apart from less common forms of dementedness . Its distinguish lineament is the presence of amyloid genus Beta plaques on the brain that spread as the disease get on . Most experimental drug break dance up the plaques . However , there has always been a minority of neuroscientist who see the plaques as a symptom , not the underlying causal agency of Alzheimer ’s . The failure of plaque - dispersing drug has give strength to their calls for alternative approach shot , ordinarily in trying to cut off the range of mountains of events that trigger off the plaque construct up .
Professor Stephen Strittmatterof Yale University is pursuing one choice by looking at the signaling mechanism that triggers plaque establishment . He go for disrupting the fundamental interaction between the protein PrPCand amyloid genus Beta would prevent the onset of Alzheimer ’s .
Strittmatter and his colleagues screen 2,560 exist drugs and 10,000 other molecules for their potential , and the clear stand - out was cefixime , which is an antibiotic still used for clap and pneumonia ( despite sound like a character from the Asterix cartoons ) .
Further testing indicated cefixime itself does not function as necessary . However , over several day at room temperature cefixime degrades into a polymer that does indeed cut off amyloid beta / PrPCinteractions .
The Yale squad make more efficient versions of the polymer , peculiarly with the capacity to queer the rake - genius barrier . They herald inCell Reportsthese not only prevent mice from developing dementedness , but actually give them space to repair their brains so their ability to navigate through a maze by memory ameliorate .
PrPCis aprion , the bizarre category of protein that cause Creutzfeldt - Jakob and harebrained Cow Disease , so Strittmatter tested his polymer in cells infect with Creutzfeldt - Jakob prion . It appeared similarly effective , although the ultimate success rate of drug screen only in cell cultures is much lower than for those that have also worked on animals .
It is always a tenacious , slow cognitive process for drug to make their way from animal examination to clinical use , and as the history of Alzheimer ’s therapy shows , one often littered with failure . However , the process is substantially shorter where drugs have already been put to other intent and shown to be dependable . Unlike cefixime , Strittmatter ’s optimized polymer has n’t had this examination , but the base record of several closely come to drugs raises hopes it will testify safe .
