Print

Print


  This message is in MIME format.  The first part should be readable text,
  while the remaining parts are likely unreadable without MIME-aware tools.
 
--PART-BOUNDARY=.19510020846.ZM21463.jethro
Content-Type: TEXT/PLAIN; CHARSET=iso-8859-1
Content-Transfer-Encoding: QUOTED-PRINTABLE
Content-Description: Text
 
 
I did a WWW search using WebCrawler for "NADH Parkinson" and got the
following. I appears very technical and I dont undrestand most of it, but
it seems to be about identifying (post humously?) Parkinson disease...=20
 
Will the experts please review this and give their  interpretation?
 
 
  NEUROGENETICS
 
           NADH DEHYDROGENASE AND CYP2D6 GENOTYPES IN PARKINSON'S DISEASE
 
S. K=F6sel, N.M. Schnopp, R. Egensperger, P. Mehraein and M.B. Graeber
 
   Molecular Neuropathology Laboratory and Reference Center for
   Neurodegenerative Disorders, Institute of Neuropathology,
   Ludwig-Maximilians-University, Thalkirchner Str. 36, 80337 Munich, Germa=
ny
 
   2nd Workshop Neurogenetics in Germany, Munich, October 19-21, 1995
 
   Abstract
   Several mutations of mitochondrial DNA (mtDNA) and polymorphisms of the
   debrisoquine 4-hydroxylase gene (CYP2D6) have been associated with an
   increased susceptibility to Parkinson's disease (PD). We have studied 21
   neuropathologically verified cases of PD and 89 controls. Genomic DNA wa=
s
   extracted from formalin-fixed, paraffin-embedded brain tissue as well as
   from freshly frozen tissue blocks and amplified using the polymerase cha=
in
   reaction. PCR products were analyzed by restriction enzyme digestion and
   direct non-radioactive cycle sequencing. Degrees of mtDNA heteroplasmy w=
ere
   determined using laser densitometry. Ratios of mtDNA carrying the 4977 b=
p
   "common deletion" were quantified by competitive PCR. 4 out of 21 PD bra=
ins
   (5/77 controls) showed a heteroplasmic mtDNAG5460A transition which affe=
cts
   the ND2 subunit gene of complex I. Degrees of heteroplasmy for this poin=
t
   mutation ranged from less than 5 to more than 95%. One PD brain was
   homoplasmic for the mtDNAA4336G transition affecting the mitochondrial
   tRNAGln. In contrast, levels of the 4977 bp deletion were not increased =
in
   the substantia nigra of PD brains. Allelic frequencies at the CYP2D6 loc=
us
   (CYP2D6G1934A and CYP2D6C2938T) were comparable in PD cases and controls=
.
   One PD brain was homozygous for the CYP2D6C2938T allele. Our results sho=
w
   that patients with Lewy-body parkinsonism exhibit genetic heterogeneity =
at
   candidate susceptibility loci. Our findings are in line with the concept
   that a definable number of interindividually variable genetic defects ma=
y
   confer increased susceptibility to PD. Systematic sequencing studies wil=
l
   help to clarify whether mitochondrial point mutations are responsible fo=
r
   the complex I defect observed in PD.
 
   Supported by the Deutsche Forschungsgemeinschaft (Gerhard Hess-Programm)=
.
 
   Headings
   Parkinson's disease (PD)
   NADH dehydrogenase
   CYP2D6 genotypes
 
 
 
   For further information please contact:
 
 
 
 
 
     ______________________________________________________________________
 
   Back HUM-MOLGEN
     ______________________________________________________________________
 
    Posted by: (Zollmann) Host: andros.informatik.uni-rostock.de date:
    September 06, 95 13:51:33
    Generated by meetings and positions 1.0 by Kai Garlipp
 
Betti & Eric M. Adams [log in to unmask]
--PART-BOUNDARY=.19510020846.ZM21463.jethro--