[11C]PIB binding in Parkinson's disease dementia

Walter Maetzler, Matthias Reimold*, Inga Liepelt, Christoph Solbach, Thomas Leyhe, Katherine Schweitzer, Gerhard W. Eschweiler, Michel Mittelbronn, Alexandra Gaenslen, Michael Uebele, Gerald Reischl, Thomas Gasser, Hans Jürgen Machulla, Roland Bares, Daniela Berg

*Corresponding author for this work

Research output: Contribution to journalArticleResearchpeer-review

129 Citations (Scopus)


[11C]PIB (11C-6-OH benzothiazole) reflects the regional distribution of amyloid (beta-sheeted proteins) in patients with Alzheimer's disease (AD). Proteinaceous inclusions in Parkinson's disease with dementia (PDD), so-called Lewy bodies, also consist of fibrillar, misfolded proteins, chiefly α-synuclein. To test whether PDD subjects show specific amyloid binding in vivo and whether this could reflect fibrillar α-synuclein accumulation, we investigated 10 PDD subjects with [11C]PIB-PET. Radioligand binding was compared to that in 11 control and 6 AD subjects. Furthermore, postmortem sections of 4 patients with Parkinson's disease (PD), therefrom 2 with dementia (PDD), and of 6 controls were stained with PIB to evaluate the histological distribution of the fluorescent ligand in the brainstem. In PET, only 2 PDD patients displayed increased PIB binding to cortical amyloid comparable to AD patients. The other 8 patients showed control-like cortical findings but elevated PIB binding in the pons and mesencephalon. Fluorescence microscopy showed PIB binding to Lewy bodies and neuromelanin in the substantia nigra of PD and PDD brainstem sections, but not in controls. These data suggest that PIB-PET can be used to further differentiate PDD with respect to cortical amyloid. Furthermore, we provide evidence that - in addition to nonspecific binding - PIB uptake in the brainstem may also reflect PDD related amyloid.

Original languageEnglish
Pages (from-to)1027-1033
Number of pages7
Issue number3
Publication statusPublished - 1 Feb 2008
Externally publishedYes


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