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> the document you refer to is not attached


it came on Raylin's message.
here it is:

Neuropathol Appl Neurobiol. 2007 Dec;33(6):599-614. Epub 
  > 2007 Oct 24.
  >   Parkinson's disease: a dual-hit hypothesis.
  >   Hawkes CH, Del Tredici K, Braak H.
  >   Essex Neuroscience Centre, Queen's Hospital, Romford, 
  > Essex UK.
  > 
  >       Accumulating evidence suggests 
  > that sporadic Parkinson's disease has a long prodromal period 
  > during which several non-motor features develop, in particular, 
  > impairment of olfaction, vagal dysfunction and sleep disorder. 
  > Early sites of Lewy pathology are the olfactory bulb and enteric 
  > plexus of the stomach. We propose that a neurotropic pathogen, 
  > probably viral, enters the brain via two routes: (i) nasal, with 
  > anterograde progression into the temporal lobe; and (ii) 
  > gastric, secondary to swallowing of nasal secretions in saliva. 
  > These secretions might contain a neurotropic pathogen that, 
  > after penetration of the epithelial lining, could enter axons of 
  > the Meissner's plexus and, via transsynaptic transmission, reach 
  > the preganglionic parasympathetic motor neurones of the vagus 
  > nerve. This would allow retrograde transport into the medulla 
  > and, from here, into the pons and midbrain until the substantia 
  > nigra is reached and typical aspects of disease commence. 
  > Evidence for this theory from the perspective of olfactory and 
  > autonomic dysfunction is reviewed, and the possible routes of 
  > pathogenic invasion are considered. It is concluded that the 
  > most parsimonious explanation for the initial events of sporadic 
  > Parkinson's disease is pathogenic access to the brain through 
  > the stomach and nose - hence the term 'dual-hit'.
  > 
maryse

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