Scientific background
Inherited manganese transporter defects (HMNDYT1/2), caused by mutations in SLC30A10 and SLC39A14, lead to brain manganese accumulation, severe neurodisability, and premature death. Current treatment with intravenous Na₂CaEDTA is burdensome, requiring monthly hospitalisation and offering limited efficacy. More effective, patient-friendly therapies are urgently needed.
We are developing two novel therapeutic approaches: (1) JD156, a manganese-selective chelator with 1,000-fold higher binding affinity than Na₂CaEDTA, and (2) lipid nanoparticle (LNP)-encapsulated SLC30A10 mRNA.
To advance clinical translation, we need to confirm therapeutic efficacy and establish a blood-based biomarker assay to monitor treatment response.
Techniques and skills to be developed
52Mn positron emission tomography (PET), mass spectrometry (MS) approaches; bioinformatic analysis of omics data; mouse husbandry and manipulation; immunohistochemistry, confocal imaging; molecular biology.
Aims of the project
This multidisciplinary project aims to advance our understanding of the molecular mechanisms underlying manganese neurotoxicity and improve therapeutic strategies.
Objectives
Year 1-3: Confirm rescue of manganese kinetics using PET.
We have already shown that manganese flux is impaired in Slc30a10KO/KO mice. Using 52Mn-PET the student will determine whether JD156/LNP-mRNA can normalise in vivo manganese kinetics. In parallel, the extent of organ delivery of JD156/LNP-mRNA can be assessed.
Year 1: Identify proteomic and lipidomic biomarkers for HMNDYT1/2.
In collaboration with the UCL GOS ICH-Biological Mass Spectrometry Centre, the student will perform untargeted proteomics and targeted lipidomics on
1. Dried blood spots from patients with HMNDYT1/2.
2. Brains from Slc30a10KO/KO mice untreated and treated with JD156/LNP-mRNA.
Year 2-3: Develop and validate a targeted biomarker assay in patient blood spots.
A selection of biomarkers will be made and a targeted LC-MS/MS assay in dried blood spots developed. This will be validated in treated Slc30a10KO/KO mice, comparing assay results with tissue manganese, haemoglobin, and histopathology.
Year 4: Identify novel regulators/effectors of manganese homeostasis/neurotoxicity.
Proteomic and lipidomic changes are expected to elucidate molecular pathways of manganese neurotoxicity. In the final year, the student will be able to interrogate molecular targets using e.g. immunohistochemistry, Western blotting, CRISPR/Cas9 etc.
Thus, this work opens an avenue for translational research including identification of new therapeutic targets, biomarkers and novel therapies for metal transport disorders.
Rotation project
Using existing proteomic and transcriptomic data from Slc30a10KO/KO mice, the student will validate novel manganese homeostasis or neurotoxicity candidates via qPCR, Western blotting and immunohistochemistry. This will lay the foundation for the PhD project by allowing the student to familiarise themselves with existing omics data and acquire key project-specific skills.
