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Cerebral Amyloid Deposition and Serotoninergic Innervation in Parkinson Disease

Vikas Kotagal, MD; Nicolaas I. Bohnen, MD, PhD; Martijn L. T. M. Müller, PhD; Robert A. Koeppe, PhD; Kirk A. Frey, MD, PhD; Roger L. Albin, MD
Arch Neurol. 2012;69(12):1628-1631. doi:10.1001/archneurol.2012.764.
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Background  Prior studies suggest that serotoninergic neurotransmission reduces β-amyloid (Aβ) production.

Objective  To determine whether serotoninergic system degeneration in Parkinson disease promotes Aβ deposition, using in vivo positron emission tomographic probes of serotonin system integrity and Aβ deposition.

Design, Setting, and Patients  Cross-sectional study of 13 subjects with Parkinson disease from the movement disorders clinics at the University of Michigan Health System and Veterans Affairs Ann Arbor Healthcare System, with positron emission tomography using the serotonin transporter ligand carbon 11 ([11C])–labeled 3-amino-4-(2-dimethylaminomethyl-phenylsulfaryl)-benzonitrile (DASB) and the Aβ ligand [11C]Pittsburgh compound B.

Results  Inverse correlations were found between DASB and Pittsburgh compound B distribution volume ratios in the neocortex (ρ = −0.577; P = .04) and striatum (ρ = −0.780; P = .002).

Conclusion  Serotoninergic system degeneration in Parkinson disease may promote the development of cerebral amyloidopathy.

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Grahic Jump Location

Figure. Scatterplots depicting the relationships between carbon 11 ([11C])–labeled 3-amino-4-(2-dimethylaminomethyl-phenylsulfaryl)-benzonitrile (DASB; serotonin transporter measure) and [11C]Pittsburgh compound B (PiB; amyloid measure) distribution volume ratios (DVRs) in the neocortex (A) and striatum (B).

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