Imperial College London
Alternate

ProfessorRogerGunn

Faculty of Medicine, Department of Brain Sciences

Emeritus Professor of Molecular Neuroimaging
 
 
 
//

Contact

 

r.gunn

 
 
//

Location

 

Burlington DanesHammersmith Campus

//

Summary

 

Publications

Citation

BibTex format

@article{Wilson:2019:10.1016/S1474-4422(19)30140-1,
author = {Wilson, H and Dervenoulas, G and Pagano, G and Koros, C and Yousaf, T and Picillo, M and Polychronis, S and Simitsi, A and Giordano, B and Chappell, Z and Corcoran, B and Stamelou, M and Gunn, RN and Pellecchia, MT and Rabiner, EA and Barone, P and Stefanis, L and Politis, M},
doi = {10.1016/S1474-4422(19)30140-1},
journal = {Lancet Neurology},
pages = {748--759},
title = {Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study},
url = {http://dx.doi.org/10.1016/S1474-4422(19)30140-1},
volume = {18},
year = {2019}
}
Download

RIS format (EndNote, RefMan)

TY  - JOUR
AB  - BACKGROUND: Because of the highly penetrant gene mutation and clinical features consistent with idiopathic Parkinson's disease, carriers of the autosomal dominant Ala53Thr (A53T; 209G→A) point mutation in the α-synuclein (SNCA) gene are an ideal population to study the premotor phase and evolution of Parkinson's pathology. Given the known neurochemical changes in the serotonergic system and their association with symptoms of Parkinson's disease, we hypothesised that carriers of the A53T SNCA mutation might show abnormalities in the serotonergic neurotransmitter system before the diagnosis of Parkinson's disease, and that this pathology might be associated with measures of Parkinson's burden. METHODS: In this cross-sectional study, we recruited carriers of the A53T SNCA mutation from specialist Movement Disorders clinics in Athens, Greece, and Salerno, Italy, and a cohort of healthy controls with no personal or family history of neurological or psychiatric disorders from London, UK (recruited via public advertisement) who were age matched to the A53T SNCA carriers. We also recruited one cohort of patients with idiopathic Parkinson's disease (cohort 1) from Movement Disorders clinics in London, UK, and retrieved data on a second cohort of such patients (cohort 2; n=40) who had been scanned with a different scanner. 7-day continuous recording of motor function was used to determine the Parkinson's disease status of the A53T carriers. To assess whether serotonergic abnormalities were present, we used [11C]DASB PET non-displaceable binding to quantify serotonin transporter density. We constructed brain topographic maps reflecting Braak stages 1-6 and used these as seed maps to calculate [11C]DASB non-displaceable binding potential in our cohort of A53T SNCA carriers. Additionally, all participants underwent a battery of clinical assessments to determine motor and non-motor symptoms and cognitive status, and [123I]FP-CIT single-photon emission CT (SPECT) to ass
AU  - Wilson,H
AU  - Dervenoulas,G
AU  - Pagano,G
AU  - Koros,C
AU  - Yousaf,T
AU  - Picillo,M
AU  - Polychronis,S
AU  - Simitsi,A
AU  - Giordano,B
AU  - Chappell,Z
AU  - Corcoran,B
AU  - Stamelou,M
AU  - Gunn,RN
AU  - Pellecchia,MT
AU  - Rabiner,EA
AU  - Barone,P
AU  - Stefanis,L
AU  - Politis,M
DO  - 10.1016/S1474-4422(19)30140-1
EP  - 759
PY  - 2019///
SN  - 1474-4422
SP  - 748
TI  - Serotonergic pathology and disease burden in the premotor and motor phase of A53T α-synuclein parkinsonism: a cross-sectional study
T2  - Lancet Neurology
UR  - http://dx.doi.org/10.1016/S1474-4422(19)30140-1
UR  - https://www.ncbi.nlm.nih.gov/pubmed/31229470
UR  - http://hdl.handle.net/10044/1/71499
VL  - 18
ER  -
Download