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Putaminal Upregulation of FosB/ΔFosB-Like Immunoreactivity in Parkinson's Disease Patients with Dyskinesia

Lindgren, Hanna S. (author)
Lund University,Basal Ganglia Pathophysiology Unit
Rylander, D. (author)
Lund University,Basal Ganglia Pathophysiology Unit
Iderberg, H. (author)
Lund University,Basal Ganglia Pathophysiology Unit
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Andersson, Malin (author)
Uppsala universitet,Institutionen för farmaceutisk biovetenskap,Neurotoxicity/Drug Safety and Toxicity
O'Sullivan, S. S. (author)
University College London,Queen Square Brain Bank
Williams, D. R. (author)
University College London,Queen Square Brain Bank
Lees, A. J. (author)
University College London,Queen Square Brain Bank
Cenci, M. A. (author)
Lund University,Basal Ganglia Pathophysiology Unit
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 (creator_code:org_t)
IOS Press, 2011
2011
English.
In: Journal of Parkinson's Disease. - : IOS Press. - 1877-7171 .- 1877-718X. ; 1:4, s. 347-357
  • Journal article (peer-reviewed)
Abstract Subject headings
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  • The transcription factor FosB is a mediator of maladaptive neuroplasticity in animal models of Parkinson´s disease (PD) and L-DOPA-induced dyskinesia. Using an antibody that recognizes all known isoforms of FosB and FosB, we have examined the expression of these proteins in post-mortem basal ganglia sections from PD patients. The patient cases were classified as being dyskinetic or non-dyskinetic based on their clinical records. Sections from neurologically healthy controls were also included in the study. Compared to both controls and non-dyskinetic cases, the dyskinetic group showed a higher density of FosB/ FosB-immunopositive cells in the posterior putamen, which represents the motor region of the striatum in primates. In contrast, the number of FosB/ FosB-positive cells did not differ significantly among the groups in the caudate, a region primarily involved with the processing of cognitive and limbic-related information. Only sparse FosB/ FosB immunoreactivity was found in the in the pallidum externum and internum, and no significant group differences were detected in these nuclei. The putaminal elevation of FosB/ FosB-like immunoreactivity in patients who had been affected by L-DOPA-induced dyskinesia is consistent with results from both rat and non-human primate models of this movement disorder. The present findings support the hypothesis of an involvement of FosB-related transcription factors in the molecular mechanisms of L-DOPA-induced dyskinesia.

Subject headings

MEDICIN OCH HÄLSOVETENSKAP  -- Klinisk medicin -- Neurologi (hsv//swe)
MEDICAL AND HEALTH SCIENCES  -- Clinical Medicine -- Neurology (hsv//eng)

Keyword

Motor complications
immediate-early genes
striatonigral
striatopallidal
medium-spiny neurons
neurodegenera- tion
dopaminergic therapies
Neurology
Neurologi

Publication and Content Type

ref (subject category)
art (subject category)

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