What does this mean in plain English? that LB is not a natural outcome of 
PD?

-----Original Message----- 
From: mschild
Sent: Wednesday, January 11, 2012 1:51 AM
To: [log in to unmask]
Subject: Study finds no support for primary pathogenic role of LBs in PD

Findings published in the Journal of Parkinson's Disease
The pathology of Parkinson's disease is characterized by a loss of 
dopamine-producing neurons in the pars compacta of the substantia nigra 
(SN), an area of the brain associated with motor control, along with the
development of α-synuclein (αS) protein in the form of Lewy bodies (LB) in 
the neurons that survive. The spread of LB pathology is thought to progress 
along with the clinical course of Parkinson's disease, although recent
studies suggest that they are not the toxic cause of cell death. A new study 
published in The Journal of Parkinson's Disease finds no support for a 
primary pathogenic role of LBs, as neither their distribution nor density 
was
associated with the severity of nigral cell loss.
"We investigated the relationship between nigral dopaminergic cell loss, 
distribution and density of α-synuclein immunoreactive LBs, and the duration 
of motor symptoms in 97 patients with Parkinson's disease," explains lead
investigator Andrew J. Lees, MD, of Queen Square Brain Bank for Neurological 
Disorders and the Reta Lila Weston Institute for Neurological Studies, UCL 
Institute of Neurology, London, UK. "Despite the reasonably close
correlation between neuronal density in SN and severity of bradykinesia and 
rigidity in Parkinson's disease, our results suggest that nigral cell loss 
is gradual and there is considerable variability, which may explain the 
clinical
heterogeneity."
Researchers confirmed that both neuronal number and density in SN in 
Parkinson's disease decrease over time. The density of nigral neurons was 
estimated to decrease by 2% each year after confirmation of the clinical
diagnosis of Parkinson's disease, but showed marked heterogeneity across 
patients. Some patients with longer duration of illness still had a 
significant number of preserved nigral neurons at the time of death. An 
average of
15% of surviving nigral neurons contained LBs and the age-adjusted 
proportion of LB-bearing neurons appeared relatively stable through the 
disease duration. "This could be explained by a passive 'one-pass' 
phenomenon
where the LBs appear at the beginning of the disease and then decrease at 
the same rate as nigral neurons are lost, or alternatively that a dynamic 
'turnover' occurs with some LBs continuously produced and destroyed at
the same rate," explains Dr. Lees.
Nigral neuron density was unrelated to the Braak PD stage of the disease 
(i.e. distribution of LBs in the brain) or to cortical LB densities. "In our 
view, the fact that neither the widespread regional distribution of LBs nor
increased cortical LB densities were found directly linked with pars 
compacta nigral cell loss lends support to the view that they are not the 
primary cause of the pathological process leading to cell death in 
vulnerable regions
in the brain in Parkinson's disease," concludes Dr. Lees.
http://www.news-medical.net/news/20120110/Study-finds-no-support-for-primary-pathogenic-role-of-LBs-in-PD.aspx

maryse

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