Updated project metadata. The glycine-51 (G51) codon in exon 3 of the rat Snca gene, encoding alpha-synuclein, was mutated to aspartic acid using CRISPR/Cas9 to generate the SncaG51D rat model of Parkinson’s (Morley et al. 2023). The G51D mutation causes an aggressive form of Parkinson’s and dementia with Lewy bodies in humans. The brains from four 6-month old rats of wild-type, heterozygous, and homozygous genotypes (Snca+/+, SncaG51D/+ and SncaG51D/G51D) were harvested and all 12 brains were bisected down the midline. Frontal cortex was isolated from one half, and synaptosomes were prepared from the other half. Following quality control the samples were processed for TMT-mass spectrometry by the Fingerprints Facility, University of Dundee. MaxQuant Version 1.6.0.16 was used for the assignment of peptides to protein using the uniport-rat-jan2018.fasta file. Pairwise comparisons were made between the different mutant samples and Snca+/+ for both the cortical and synaptosome samples. Morley V, Dolt KS, Alcaide-Corral CJ, Walton T, Lucatelli C, Mashimo T, Tavares AAS & Kunath T (2023) In vivo18F-DOPA PET imaging identifies a dopaminergic deficit in a rat model with a G51D α-synuclein mutation. Front. Neurosci. 17, 1095761.