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   Epidemic spreading and neurodegenerative progression   
      
   Last updated: 20 November 2014 at 11am PST   
      
   Neurology / Neuroscience   
   Biology / Biochemistry   
   Alzheimer's / Dementia   
      
      
      
   Researchers from the Montreal Neurological Institute have used a model   
   inspired by patterns of epidemic disease spreading to map how misfolded   
   proteins propagate within the brain.   
      
   Proteins which fail to configure correctly (misfolded proteins) are associated   
   with aging and several human neurodegenerative diseases, such as Alzheimer's.   
   In research published in PLOS Computational Biology, Yasser Iturria Medina and   
   colleagues analyze    
   over 700 individual Amyloid-beta proteins imaging datasets to conclude that   
   the propagation of these misfolded proteins, associated with Alzheimer's   
   disease progression, can be mathematically described by the interaction   
   between infection-like agents (   
   the misfolded proteins) and the brain's defense response.   
      
   The authors' model relies on the striking similarity between intra-brain   
   pathology propagation processes and the spread of human infectious diseases.   
   They demonstrate that the brain's connections between cells play a similar   
   role in misfolded protein    
   dynamics as global air-traffic routes play for the international spreading of   
   diseases such as the 2009 H1N1 pandemic. The researchers also identified   
   genetic and demographic factors that influence this phenomenon in healthy   
   aging and Alzheimer's disease    
   progression.   
      
   The authors said: "The epidemic spreading theory constitutes a general   
   framework for intra-brain region-to-region transference mechanisms in health   
   and disease. Our next goal is to uncover how other pathologic factors, such as   
   vascular dysregulation,    
   interact with misfolded protein propagation in causing dementia. Identifying   
   aberrant individual clearance levels as a major factor in Amyloid-beta   
   proteins accumulation, as opposed to increased production levels, could imply   
   a turning point for the    
   development of therapeutic strategies in Alzheimer's disease."   
      
   Adapted by MNT from original media release   
      
      
   http://www.medicalnewstoday.com/releases/285712.php?tw   
      
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