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   Scientific American            
      
      
   Nature    
   NEUROSCIENCE    
      
   More Evidence Emerges for "Transmissible Alzheimer's" Theory    
      
      
   The disease is not normally infectious, but people who received grafts from   
   cadavers did show telltale markers in their brains    
   By Alison Abbott, Nature magazine on January 26, 2016    
      
   Deposits of amyloid-β protein (brown) in the frontal cortex of patients who   
   developed CJD after surgery.    
   Frontzek K, Lutz MI, Aguzzi A, Kovacs GG, Budka H.    
      
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   For the second time in four months, researchers have reported autopsy results   
   that suggest Alzheimer’s disease might occasionally be transmitted to people   
   during certain medical treatments—although scientists say that neither set   
   of findings is    
   conclusive.    
   The latest autopsies, described in the Swiss Medical Weekly on January 26,   
   were conducted on the brains of seven people who died of the rare,   
   brain-wasting Creutzfeldt–Jakob disease (CJD). Decades before their deaths,   
   the individuals had all received    
   surgical grafts of dura mater—the membrane that covers the brain and spinal   
   cord. These grafts had been prepared from human cadavers and were contaminated   
   with the prion protein that causes CJD.    
   But in addition to the damage caused by the prions, five of the brains   
   displayed some of the pathological signs that are associated with   
   Alzheimer’s disease, researchers from Switzerland and Austria report.   
   Plaques formed from amyloid-β protein were    
   discovered in the grey matter and blood vessels. The individuals, aged between   
   28 and 63, were unusually young to have developed such plaques. A set of 21   
   controls, who had not had surgical grafts of dura mater but died of sporadic   
   CJD at similar ages,    
   did not have this amyloid signature.    
   Transplant trouble    
   According to the authors, it is possible that the transplanted dura mater was   
   contaminated with small ‘seeds’ of amyloid-β protein—which some   
   scientists think could be a trigger for Alzheimer’s—along with the prion   
   protein that gave the    
   recipients CJD.    
   Both diseases have long incubation periods. But whereas CJD progresses quickly   
   once initiated, age-related Alzheimer’s develops slowly. None of the   
   individuals had displayed obvious Alzheimer’s symptoms before their deaths.    
   The results follow a study published in Nature last September in which   
   scientists from University College London reported that four of eight   
   relatively young people, all of whom died of CJD decades after receiving   
   contaminated batches of growth hormone    
   prepared from cadavers, also displayed amyloid plaques in the blood vessels   
   and grey matter of their brains.    
   “Our results are all consistent,” says neurologist John Collinge, a   
   co-author on the Nature paper. “The fact that the new study shows the same   
   pathology emerging after a completely different procedure increases our   
   concern.”    
   Not infectious    
   Neither study implies that Alzheimer’s disease could ever be transmitted   
   through normal contact with caretakers or family members, the scientists   
   emphasize. And no one uses cadaver-derived preparations in the clinic anymore.   
   Synthetic growth hormone is    
   used for growth disorders, and synthetic membranes are used for patching up in   
   brain surgery.    
   But the scientists say that if the theory of amyloid seeding turns out to be   
   true, it would have important clinical implications. In general surgery, for   
   example, any amyloid-β proteins, which are very sticky, would not be   
   routinely removed from    
   surgical instruments; standard sterilization procedures cannot shift them.    
   “It is our job as doctors to see in advance what might become a problem in   
   the clinic,” says neuropathologist Herbert Budka of the University Hospital   
   Zurich, Switzerland, who is a co-author of the latest paper.    
   “Nothing is proven yet,” cautions Pierluigi Nicotera, head of the German   
   Centre for Neurodegenerative Diseases in Bonn. He points out that amyloid-β   
   has not been identified in the preparations that were transplanted in either   
   the growth hormone or    
   dura mater studies. Nor can researchers rule out the possibility that the   
   underlying condition that led to the need for neurosurgery could have   
   contributed to the observed amyloid pathology, as the authors of the latest   
   paper note.    
   “We need more systematic studies in model organisms to work out if the   
   seeding hypothesis of Alzheimer’s is correct,” Nicotera says.    
   This article is reproduced with permission and was first published on January   
   26, 2016.    
      
      
      
      
   http://www.scientificamerican.com/article/more-evidence-emerges-   
   or-transmissible-alzheimer-s-theory/    
      
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