Abstract #1303

in vivo longitudinal imaging unravels the origin of neuromelanin-MRI contrast in a rat model of Parkinson’s disease

Jean-Baptiste Perot¹, Anthony Ruze², Sana Rebbah³, Capucine Cadin¹, Arnaud Le Troter⁴, Lucas Soustelle⁴, Laura Mouton², Romain Valabregue², Annabelle Parent⁵, Mathieu D Santin², Miquel Vila⁵, and Stéphane Lehéricy^1,2

¹Paris Brain Institute – ICM, MOVIT team, Sorbonne Université, Inserm U1127, CNRS 7225, Hôpital Pitié-Salpêtriere, Paris, France, ²Paris Brain Institute – ICM, Centre de NeuroImagerie de Recherche – CENIR, Sorbonne Université, Inserm U1127, CNRS 7225, Hôpital Pitié-Salpêtriere, Paris, France, ³Paris Brain Institute – ICM, Data Analysis Core, Sorbonne Université, Inserm U1127, CNRS 7225, Hôpital Pitié-Salpêtriere, Paris, France, ⁴Aix-Marseille Univ, CRMBM, CNRS UMR 7339, APHM, La Timone Hospital, CEMEREM, Marseille, France, ⁵Neurodegenerative Diseases Research Group, Vall d’Hebron Research Institute (VHIR)-Network Center for Biomedical Research in Neurodegenerative Diseases (CIBERNED), Barcelona, Spain

Synopsis

Keywords: Novel Contrast Mechanisms, Contrast Mechanisms

Motivation: Neuromelanin-MRI contrast is a promising biomarker for Parkinson's disease, but still needs investigation as the biological and physical origins of the contrast are still unclear.

Goal(s): The objective was to unravel the mechanisms behind neuromelanin-MRI contrast, both biologically and physically, and to better understand the role of neuromelanin in Parkinson's disease.

Approach: We performed in vivo longitudinal neuromelanin-MRI coupled with quantitative multiparametric imaging on a rat model of Parkinson's disease based on accumulation of neuromelanin, with histological validation.

Results: Results show that contrast increases with neuromelanin accumulation and decreases with neuronal loss. The contrast arises from T₁ reduction due to paramagnetic neuromelanin-iron complexes.

Impact: We provide first in vivo validation and better understanding of neuromelanin-MRI as a biomarker of neuronal loss in Parkinson's disease. Results also suggest a pathogenic threshold of neuromelanin accumulation triggering neurodegeneration. Investigating this hypothesis may lead to new therapeutic window.

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