Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease

Aldo Quattrone; Antonio Bagnato; Grazia Annesi; Fabiana Novellino; Letterio Morgante; Giovanni Savettieri; Mario Zappia; Patrizia Tarantino; Innocenza Claudia Cirò Candiano; Ferdinanda Annesi; Donatella Civitelli; Francesca Emanuela Rocca; Marco D'Amelio; Giuseppe Nicoletti; Maurizio Morelli; Alfredo Petrone; Piercostanzo Loizzo; Francesca Condino

doi:10.1002/mds.21701

Myocardial 123metaiodobenzylguanidine uptake in genetic Parkinson's disease

Mov Disord. 2008 Jan;23(1):21-7. doi: 10.1002/mds.21701.

Authors

Aldo Quattrone¹, Antonio Bagnato, Grazia Annesi, Fabiana Novellino, Letterio Morgante, Giovanni Savettieri, Mario Zappia, Patrizia Tarantino, Innocenza Claudia Cirò Candiano, Ferdinanda Annesi, Donatella Civitelli, Francesca Emanuela Rocca, Marco D'Amelio, Giuseppe Nicoletti, Maurizio Morelli, Alfredo Petrone, Piercostanzo Loizzo, Francesca Condino

Affiliation

¹ Institute of Neurology, University Magna Graecia, Catanzaro, Italy. [email protected]

PMID: 17975812
DOI: 10.1002/mds.21701

Abstract

Myocardial (123)Metaiodobenzylguanidine (MIBG) enables the assessment of postganglionic sympathetic cardiac innervation. MIBG uptake is decreased in nearly all patients with Parkinson's disease (PD). Our objective was to evaluate MIBG uptake in patients with genetic PD. We investigated MIBG uptake in 14 patients with PD associated with mutations in different genes (Parkin, DJ-1, PINK1, and leucine-rich repeat kinase 2 -LRRK2), in 15 patients with idiopathic PD, and 10 control subjects. The myocardial MIGB uptake was preserved in 3 of the 4 Parkin-associated Parkinsonisms, in 1 of the 2 patients with DJ-1 mutations, in 1 of the 2 brothers with PINK1 mutations, in 3 of the 6 unrelated patients with Gly2019Ser mutation in the LRRK2 gene, whereas it was impaired in all patients with idiopathic PD. MIBG was preserved in all control subjects. Our study shows that myocardial MIGB uptake was normal in 8 of 14 patients with genetic PD, suggesting that cardiac sympathetic denervation occurs less frequently in genetic PD than in idiopathic PD. Our findings also demonstrate that MIGB uptake has a heterogeneous pattern in genetic PD, because it was differently impaired in patients with different mutations in the same gene or with the same gene mutation.

2007 Movement Disorder Society

Publication types

Comparative Study

MeSH terms

3-Iodobenzylguanidine / pharmacokinetics*
Adult
DNA Mutational Analysis
Diagnosis, Differential
Female
Galvanic Skin Response / physiology
Genotype
Humans
Intracellular Signaling Peptides and Proteins / blood
Intracellular Signaling Peptides and Proteins / genetics
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
Male
Middle Aged
Movement Disorders / diagnosis
Movement Disorders / epidemiology
Myocardium / metabolism*
Oncogene Proteins / blood
Oncogene Proteins / genetics
Parkinson Disease / diagnosis*
Parkinson Disease / epidemiology
Parkinson Disease / genetics*
Parkinsonian Disorders / diagnosis*
Parkinsonian Disorders / epidemiology
Parkinsonian Disorders / genetics*
Point Mutation / genetics*
Promoter Regions, Genetic
Protein Deglycase DJ-1
Protein Kinases / blood
Protein Kinases / genetics
Protein Serine-Threonine Kinases / blood
Protein Serine-Threonine Kinases / genetics
Radiopharmaceuticals / pharmacokinetics*
Severity of Illness Index
Surveys and Questionnaires
Tomography, Emission-Computed, Single-Photon / methods
Ubiquitin-Protein Ligases / blood
Ubiquitin-Protein Ligases / genetics

Substances

Intracellular Signaling Peptides and Proteins
Oncogene Proteins
Radiopharmaceuticals
3-Iodobenzylguanidine
Ubiquitin-Protein Ligases
parkin protein
Protein Kinases
LRRK2 protein, human
Leucine-Rich Repeat Serine-Threonine Protein Kinase-2
PTEN-induced putative kinase
Protein Serine-Threonine Kinases
PARK7 protein, human
Protein Deglycase DJ-1