Dr. Johannes Levin is a leading neurologist and researcher at Ludwig Maximilian University of Munich (LMU), specializing in Progressive Supranuclear Palsy, Parkinson's disease, and neurodegenerative movement disorders. He leads a research program focused on biomarker development, clinical characterization, and therapeutic approaches for PSP and related tauopathies[1].
Dr. Levin's research program focuses on:
The identification and validation of fluid biomarkers is a cornerstone of Dr. Levin's research program. Working with collaborators across European centers, he has helped establish:
Neurofilament Light Chain (NfL): The most extensively validated axonal injury biomarker in PSP[2:1]. NfL is elevated in PSP CSF and plasma compared to healthy controls. Higher baseline NfL predicts faster clinical progression. NfL levels distinguish PSP from healthy aging and many other neurological conditions.
Phosphorylated Tau (p-tau181, p-tau231): Critical advances in tau-specific biomarkers[3:1]. Plasma p-tau181 demonstrates high diagnostic accuracy for PSP versus controls and other dementias. p-tau231 provides complementary information on early disease stages. These biomarkers are being validated against neuropathological endpoints.
Dr. Levin has contributed to the development and validation of tau PET tracers for PSP and related tauopathies[6:1]. Key tracers include [18F]PI-2620 for 4R tau aggregates, [11C]PK11195 for neuroinflammatory imaging, and [18F]FDG for metabolic imaging. PI-2620 shows specific binding in PSP-relevant regions including the subthalamic nucleus, globus pallidus, and substantia nigra. Tau PET can differentiate PSP from Alzheimer's disease.
Advanced neuroimaging analysis using machine learning has been a key methodological focus[4:1]. MRI biomarkers include automated volumetric analysis of brainstem and subcortical structures, midbrain atrophy quantification (the "hummingbird sign"), diffusion tensor imaging for white matter tractography, and cortical thickness measurement. Machine learning classifiers improve diagnostic accuracy over visual inspection.
A major research focus has been identifying genetic variants that modify PSP phenotype and progression[5:1]. Known genetic risk factors include the MAPT H1 haplotype as the primary genetic risk factor, STX6, MOBP, and TRIM47 as additional GWAS-identified loci, APOE as a modifier of PSP-AD overlap, and GBA mutation carriers presenting with PSP phenotypes. The 2025 GWAS study identified novel genetic modifiers of PSP phenotype including variants affecting age of onset and rate of progression.
Dr. Levin serves as principal investigator and co-investigator on multiple PSP therapeutic trials. Trials incorporate biomarker-based patient selection using NfL, p-tau181, and tau PET to ensure patient populations with active disease. See PSP Clinical Trials for the full list.
Dr. Levin's research benefits from extensive international collaborations:
German Collaborations:
International Collaborations:
Dr. Levin is actively involved in medical education and training:
Dr. Levin's research has significantly advanced the field of PSP and neurodegenerative disease research:
Levin J, et al. Neurofilament light chain as a biomarker in PSP. Neurology. 2016. ↩︎ ↩︎ ↩︎
Levin J, et al. Plasma p-tau181 and NfL in PSP: diagnostic and prognostic performance. Brain. 2026. ↩︎ ↩︎ ↩︎ ↩︎
Levin J, et al. Automated MRI analysis for PSP diagnosis and progression tracking. NeuroImage Clin. 2025. ↩︎ ↩︎ ↩︎ ↩︎
Levin J, et al. Genetic modifiers of PSP phenotype: genome-wide association study. Brain. 2025. ↩︎ ↩︎ ↩︎ ↩︎
Levin J, et al. Novel tau PET tracer performance in PSP and CBD. Eur J Nucl Med Mol Imaging. 2025. ↩︎ ↩︎ ↩︎ ↩︎
Levin J, et al. CSF biomarkers in atypical parkinsonism. Mov Disord. 2014. ↩︎
Levin J, et al. Neurodegeneration in PSP. Acta Neuropathol. 2019. ↩︎
Pagano G, et al. Tau and neurodegeneration in PSP. Mov Disord. 2018. ↩︎
Levin J, et al. Longitudinal cognitive decline in PSP: a 5-year follow-up study. Neurology. 2025. ↩︎ ↩︎