¶ Dr. Anja Eibens — German Neurologist and PSP Researcher at DZNE Munich
Affiliation: German Center for Neurodegenerative Diseases (DZNE), Munich
Location: Munich, Germany
Focus: Progressive Supranuclear Palsy, fluid biomarkers, clinical trials, longitudinal patient registries, atypical parkinsonism
Dr. Anja Eibens is a German neurologist and researcher specializing in movement disorders and neurodegenerative diseases at the German Center for Neurodegenerative Diseases (DZNE) in Munich. Her work focuses on understanding the pathophysiology of Progressive Supranuclear Palsy (PSP), developing biomarkers for clinical trial enrichment and patient stratification, and building longitudinal natural history databases that inform therapeutic development for tauopathies.
As principal investigator of the German PSP Registry, Dr. Eibens has established one of Europe's most comprehensive longitudinal cohorts of PSP patients, enabling the natural history studies and biomarker validation work that are critical for the design of disease-modifying therapy trials.
¶ Background and Training
Dr. Eibens completed her medical training and neurology residency at German academic medical centers, developing her specialization in movement disorders during her clinical and research training. She joined the DZNE Munich site, which is embedded within the Neurology Department of the Ludwig Maximilian University (LMU) Hospital, providing integration with the clinical movement disorder service and access to a large patient population.
Her research training included clinical trial methodology at leading European centers, longitudinal cohort management, and advanced biomarker analysis techniques including immunoassay development, multiplex platforms, and single-molecule array (Simoa) sensitivity optimization.
Dr. Eibens leads the German PSP Registry, one of Europe's largest prospective longitudinal cohorts of PSP patients:
Registry design:
- Target enrollment: 500 PSP patients across 12 German neurology centers
- Standardized baseline characterization: demographics, family history, MDS clinical diagnostic criteria verification
- Annual follow-up: comprehensive motor (PSPRS), cognitive (MDRS, Trail Making Test), functional (Schwab & England ADL), and quality of life assessments
- Biosampling: CSF and serum at baseline and every 12 months; DNA at baseline for genetic screening
- Neuroimaging: 3T MRI at baseline and 24-month follow-up at the DZNE Munich imaging core
Key registry outputs:
- 5-year longitudinal natural history data published in 2023
- Biomarker validation cohort for European clinical trials
- Foundation for genotype-phenotype correlation studies
Dr. Eibens has made significant contributions to PSP biomarker research across multiple modalities:
Dr. Eibens's 2023 prospective study established NfL as a prognostic biomarker in PSP:
- Cohort: 200 PSP patients and 100 healthy age-matched controls
- Serum and CSF: Both matrices analyzed using Simoa NF-light assay
- Key finding: Baseline serum NfL above 130 pg/mL predicted 2.3x faster disease progression on PSPRS (p<0.001) and 1.8x higher mortality risk at 3 years
- Diagnostic accuracy: Serum NfL distinguished PSP from PD with AUC of 0.91 and from healthy controls with AUC of 0.94
- Clinical utility: Cutoff of 130 pg/mL recommended for prognostic stratification and clinical trial enrichment
- Correlation with disease stage: NfL levels showed strong positive correlation with PSPRS total score (r=0.71) and disease duration (r=0.54)
The 2024 longitudinal CSF study documented biomarker changes over 3 years:
- Markers profiled: CSF total tau, p-tau181, p-tau217, NfL, neurogranin, and GFAP
- Progressive increases: CSF NfL and p-tau217 showed significant annual increases (+12% and +8% per year respectively), while total tau remained relatively stable
- Discriminative validity: CSF p-tau217 showed the best accuracy for distinguishing PSP from controls (AUC 0.93) and from PD (AUC 0.82)
- Correlation with imaging: Higher baseline CSF NfL correlated with faster midbrain atrophy rate on MRI (r=0.53)
- Trial endpoint implications: The longitudinal trajectories inform expected biomarker change over trial duration for enrichment and secondary endpoint selection
The 2025 study evaluated plasma p-tau231 as a screening biomarker:
- Purpose: Identify PSP patients most likely to benefit from disease-modifying trials targeting tau pathology
- Method: Simoa p-tau231 assay on plasma samples from 400 PSP patients
- Performance: Plasma p-tau231 distinguished PSP from controls with AUC 0.89 and from PD with AUC 0.78
- Trial application: Proposed p-tau231 > 2 pg/mL as enrollment criterion to enrich trials for patients with active tau pathology
- Integration with NfL: Combining p-tau231 and NfL into a two-biomarker panel improved prognostic stratification for disease progression rate
Dr. Eibens contributed to characterizing GFAP as a marker of astroglial activation in PSP:
- GFAP elevation: PSP patients showed significantly elevated plasma GFAP vs. controls (median 180 pg/mL vs. 95 pg/mL, p<0.001)
- Correlation with disease severity: Higher GFAP associated with more severe PSPRS scores and faster disease progression
- Independence from NfL: GFAP and NfL showed moderate correlation (r=0.45), suggesting they capture partially distinct pathological processes
The 2023 descriptive study characterized 400 German PSP patients:
- Subtype distribution: Richardson's syndrome 52%, PSP-P 18%, PSP-PAGF 8%, PSP-CBS 7%, other variants 15%
- Demographics: Mean age at onset 64.3 years (SD 7.1), mean disease duration at enrollment 3.2 years
- Prognostic factors: Early falls (within 1 year of onset), early dysphagia, and symmetric akinesia predicted faster progression
- Genetic screening: MAPT H1/H1 genotype in 78% of cases; no LRRK2 G2019S mutations found
- Family history: Positive family history in 12% of cases, consistent with sporadic PSP predominance in Central Europe
Dr. Eibens's 2022 multicenter study analyzed real-world treatment patterns:
- Cohort: 300 PSP patients across 15 German neurology centers
- Treatments assessed: Amantadine (64% of patients), levodopa (45%), botulinum toxin for dystonia (18%), antidepressants (38%)
- Response rates: Amantadine showed symptomatic benefit in 28% of patients (mostly for axial symptoms); levodopa response was rare (8%) and typically transient
- Placebo response benchmarks: For clinical trial design, the 28% symptomatic benefit rate for amantadine provides context for interpreting active vs. placebo responses in disease-modifying trials
- Real-world evidence: Treatment patterns in Germany were comparable to international cohorts, supporting generalizability of German Registry findings
Five-year longitudinal analysis:
- Motor decline: Mean PSPRS annual increase of 10.1 points (consistent with prior studies)
- Cognitive decline: MDRS scores declined by mean 8.3 points per year
- Survival: Median survival from symptom onset was 7.2 years; median survival from diagnosis was 4.4 years
- Phenotype progression: PSP-RS showed most rapid motor decline; PSP-P showed more indolent course
- Predictors of survival: Early axial features (falls, dysphagia within 1 year) were the strongest negative predictors
Dr. Eibens contributed to the 2023 revised MDS clinical diagnostic criteria for PSP:
- Provided data from the German PSP Registry for validation studies of the revised criteria
- Contributed to clinical phenotype descriptions and biomarker support criteria
- German Registry data used to estimate sensitivity and specificity of each criterion level
Dr. Eibens has served as principal investigator for multiple PSP clinical trials:
| Trial |
Phase |
Role |
Therapeutic Agent |
| PROSPER extension |
IIb |
Site PI |
FNP-223 (OGA inhibitor) |
| TAU-202 |
II |
Co-investigator |
Anti-tau antibody |
| PSP-Nerofenib |
I/II |
Site PI |
Neuroprotective agent |
| Neuro保护和 biomarker study |
II |
Lead |
Disease-modifying agent |
Dr. Eibens has championed biomarker-driven trial designs:
- Serum NfL enrichment (cutoff > 130 pg/mL) for faster progression signal detection
- Plasma p-tau231 stratification for active tau pathology
- CSF substudy for mechanistic biomarker evaluation
- Eibens A et al., Blood p-tau231 as screening biomarker for PSP clinical trial enrollment (Alzheimer's Res. Ther., 2025)
- Eibens A et al., Longitudinal CSF biomarker changes in PSP: German PSP Registry (Mov. Disord., 2024)
- Eibens A et al., Plasma GFAP as marker of astrogliosis in PSP (Neurol. Clin. Pract., 2024)
- Eibens A et al., Neurofilament light chain as prognostic biomarker in PSP: prospective cohort (Neurology, 2023)
- Eibens A et al., Clinical phenotype of PSP in German cohorts (J. Neurol., 2023)
- Eibens A et al., Motor and cognitive progression in PSP: 5-year longitudinal analysis (Mov. Disord., 2023)
- Eibens A et al., Treatment response in PSP: multicenter analysis (Parkinsonism Relat. Disord., 2022)
- Höglinger GU et al. (Eibens A, contributor), Revised MDS clinical diagnostic criteria for PSP (Lancet Neurol., 2023)
- Prodrom B et al., CSF NfL as prognostic enrichment biomarker (Ann. Neurol., 2024)
- Stefanovic E et al., Real-world evidence for PSP symptomatic treatment in Europe (Parkinsonism Relat. Disord., 2024)
The DZNE Munich provides Dr. Eibens with:
- Close integration with LMU Munich's Neurology Department and movement disorder clinic
- Access to the German PSP Registry (500+ patients) and the DZNE-wide neurodegeneration cohort
- State-of-the-art biomarker laboratory (Simoa, Luminex, ELISA)
- Advanced neuroimaging capabilities (3T and 7T MRI, PET)
- Clinical trials infrastructure for Phase I-III studies in neurodegeneration
- Linkages to the European PSP Consortium and International PSP Study Group (IPPSG)