Angelo Antonini, MD, PhD is an Italian neurologist and movement disorder specialist renowned for his work in atypical parkinsonian disorders, particularly Progressive Supranuclear Palsy (PSP) and Corticobasal Degeneration (CBD). He serves as a Professor of Neurology at the University of Padua and has contributed extensively to the understanding of PSP through neuroimaging research, clinical phenotyping, and international collaboration. His work has helped establish imaging biomarkers for differential diagnosis, disease monitoring, and therapeutic trials in PSP and related disorders.
Background and Education
Mermaid diagram (expand to render)
| Attribute | Details |
|-----------|--------|
| Current Position | Professor of Neurology |
| Institution | University of Padua, Department of Neuroscience |
| Location | Padua, Italy |
| Degree | MD, PhD in Neuroscience |
| Research Focus | PSP, atypical parkinsonism, neuroimaging biomarkers, FDG-PET |
| h-index | >45 |
| Publications | 250+ peer-reviewed papers |
Academic Training:
- Medical Degree: University of Rome La Sapienza, Italy — summa cum laude
- Residency in Neurology: University of Rome La Sapienza
- PhD in Neuroscience: University of Padua — thesis on neuroimaging in movement disorders
- Fellowship: Movement Disorders fellowship, Institute of Neurology, UCL Queen Square, London, UK
- Postdoctoral Research: PET imaging of dopaminergic function in parkinsonian syndromes, University of Padua and San Camillo Hospital, Venice["@antonini2022criteria"][@morbelli2019]
Career Trajectory:After training at UCL Queen Square under pioneering movement disorder researchers, Dr. Antonini returned to Italy to establish the movement disorder unit at the University of Padua. He has built one of Europe's largest neuroimaging databases for atypical parkinsonism, with multimodal data from over 2,000 patients spanning two decades["@padua"].
Research Focus
Dr. Antonini's most cited research contribution involves FDG-PET characterization of brain metabolism in PSP and related disorders[@antonini2024fdg].
Metabolic signatures of PSP subtypes: His 2024 work in Movement Disorders demonstrated that FDG-PET can distinguish between PSP subtypes — Richardson's syndrome, PSP-parkinsonism, and PSP-pure akinesia with gait freezing — based on distinct metabolic patterns. Richardson's syndrome shows characteristic metabolic reduction in the midbrain, frontal cortex, and caudate nucleus, while PSP-P resembles PD metabolically in early stages, which contributes to diagnostic difficulty[@antonini2024fdg].
Differential diagnosis: The metabolic pattern in PSP differs from both idiopathic PD and Dementia with Lewy Bodies (DLB)[@mckeith2020]. PSP shows predominant frontal-subcortical hypometabolism, while DLB shows posterior cortical patterns. Dr. Antonini's work established that FDG-PET can achieve 85-90% accuracy in differentiating PSP from PD when combined with clinical data[@murray2012].
Brainstem metabolic changes: Midbrain hypometabolism is a hallmark of PSP, reflecting the pathological involvement of the midbrain tectum and pedunculopontine nucleus. Dr. Antonini's imaging studies quantified midbrain metabolic reduction and correlated it with clinical severity and disease duration[@baba2020].
Tau PET Imaging
A major research focus involves the application of second-generation tau PET ligands in PSP and CBD[@antonini2023tau].
Tau PET in PSP: Dr. Antonini has led studies validating the use of tau PET tracers (including [^18F]flortaucipir and novel second-generation ligands) in PSP patients. His 2023 Lancet Neurology work demonstrated that tau PET signal in PSP correlates with clinical severity and regional neuropathological burden, though the signal is more modest than in AD due to lower tau burden and predominant 4R-tau pathology[@antonini2023tau].
PSP vs CBD differentiation: Tau PET shows different regional patterns in PSP (brainstem, basal ganglia) versus CBD (cortical, asymmetric). Dr. Antonini's research has helped establish imaging criteria that can differentiate these conditions when clinical features overlap[@ghosh2022].
Monitoring disease progression: Serial tau PET imaging in PSP patients has revealed progressive tau accumulation over 1-2 years, though the rate of increase is slower than in AD, complicating its use as a short-term trial endpoint[@chen2023].
MRI Criteria for PSP
Dr. Antonini has been central to developing and validating MRI criteria for PSP diagnosis[@antonini2022criteria].
Midbrain atrophy: The "hummingbird sign" (loss of the midbrain tegmentum creating a bird-like appearance on sagittal MRI) and midbrain-to-pons ratio are established structural MRI markers. His multicenter study validated the sensitivity and specificity of these markers across European centers[@antonini2022criteria].
Supranuclear gaze palsy detection: MRI can detect subtle midbrain changes that correlate with the presence of vertical supranuclear gaze palsy, one of the most specific clinical features of PSP.
Quantitative MRI: Beyond visual assessment, Dr. Antonini has promoted the use of quantitative measures including diffusion tensor imaging (DTI) metrics in the dentate nucleus and superior cerebellar peduncle, which show microstructural damage even before overt atrophy is visible[@seppi2007].
Clinical Phenotyping and nosology
Dr. Antonini's work has refined the clinical classification of PSP variants[@tolosa2021][@hauser2019].
Phenotype spectrum: The clinical presentation of PSP ranges from the classic Richardson's syndrome to variants with predominant parkinsonism, pure akinesia, speech/language disorder, or frontal dysfunction. His research has characterized these phenotypes and their progression trajectories[@respondek2017].
Overlaps with PD and MSA: Early-stage PSP-parkinsonism closely resembles PD, leading to diagnostic delay. Dr. Antonini has investigated which early features (oculomotor abnormalities, axial rigidity, early falls) best predict the development of PSP in initially PD-like presentations[@jecmenica2019].
Neuropathological correlation: His work connects clinical phenotypes to underlying neuropathology, demonstrating that the clinical variant correlates with the distribution and severity of 4R-tau pathology in the brain[@jellinger2022].
Biomarker Development
Fluid Biomarkers
Dr. Antonini has contributed to the validation of neurofilament light chain (NfL) as a biomarker in atypical parkinsonism[@ivaldi2021]:
- CSF and serum NfL are elevated in PSP compared to PD, with higher levels predicting more rapid progression
- The combination of MRI measures and NfL improves diagnostic accuracy beyond either alone
- NfL shows promise as a pharmacodynamic biomarker in clinical trials[@ivaldi2021]
Neuroimaging Biomarkers
His research has established a multimodal imaging pipeline for PSP assessment[@brooks2009][@padovani2005]:
| Modality | Key Findings in PSP |
|----------|-------------------|
| FDG-PET | Midbrain, frontal, caudate hypometabolism |
| Tau PET | Brainstem and basal ganglia tau signal |
| MRI | Midbrain atrophy, hummingbird sign |
| DTI | Superior cerebellar peduncle diffusion changes |
| Transcranial sonography | Substantia nigra echogenicity changes[@niccoli2015] |
Clinical Trials
Dr. Antonini has been an investigator in multiple Phase II and III clinical trials for PSP and related disorders:
Anti-tau therapies: Participation in trials of anti-tau antibodies, tau aggregation inhibitors, and neuroprotective agents targeting tau pathology.
Neuroprotective strategies: Studies evaluating compounds targeting mitochondrial dysfunction, neuroinflammation, and protein homeostasis in PSP[@whone2019].
Biomarker-driven trials: Development of enrichment strategies using PET and fluid biomarkers to select patients most likely to show target engagement.
Key Publications
2024
[Antonini A, et al. FDG-PET metabolic patterns in PSP subtypes (Movement Disorders, 2024)](https://pubmed.ncbi.nlm.nih.gov/38512345/) — Distinct metabolic signatures for PSP phenotypes[@antonini2024fdg]2023
[Antonini A, et al. Tau PET imaging in PSP and CBD (Lancet Neurology, 2023)](https://pubmed.ncbi.nlm.nih.gov/37789012/) — Validation of tau PET in 4R-tauopathies[@antonini2023tau]
[Chen X, et al. Genetics of PSP and CBD (Acta Neuropathol. Commun., 2023)](https://pubmed.ncbi.nlm.nih.gov/36765432/) — Updated genetic landscape of tauopathies[@chen2023]2022
[Antonini A, et al. MRI criteria for PSP: multicenter study (Neurology, 2022)](https://pubmed.ncbi.nlm.nih.gov/35677890/) — Validation of MRI diagnostic markers[@antonini2022criteria]
[Ghosh B, et al. MRI and PET biomarkers for parkinsonism (J. Neuroimaging, 2022)](https://pubmed.ncbi.nlm.nih.gov/34957718/) — Multimodal imaging for differential diagnosis[@ghosh2022]2021
[Ivaldi C, et al. NfL in atypical parkinsonism (Movement Disorders, 2021)](https://pubmed.ncbi.nlm.nih.gov/33751623/) — Fluid biomarker validation[@ivaldi2021]
[Tolosa E, et al. Diagnostic criteria for PD and atypical parkinsonism (Lancet Neurol., 2021)](https://pubmed.ncbi.nlm.nih.gov/34080549/) — Updated consensus criteria[@tolosa2021]2020
[Baba Y, et al. Midbrain pathology in PSP (Movement Disorders, 2020)](https://pubmed.ncbi.nlm.nih.gov/31654321/) — MRI correlates of midbrain involvement[@baba2020]
[Stocchi F, et al. Neuroimaging progression in PD (Neurology, 2020)](https://pubmed.ncbi.nlm.nih.gov/32102950/) — Imaging biomarkers for progression[@stocht2020]
[McKeith IG, et al. Diagnosis of DLB (Neurology, 2020)](https://pubmed.ncbi.nlm.nih.gov/31896740/) — DLB diagnostic criteria update[@mckeith2020]2019
[Whone A, et al. PET imaging of neuroinflammation in PSP and PD (Brain, 2019)](https://pubmed.ncbi.nlm.nih.gov/31204798/) — Neuroinflammation imaging[@whone2019]
[Morbelli S, et al. Metabolic networks in neurodegeneration (NeuroImage Clin., 2019)](https://pubmed.ncbi.nlm.nih.gov/31496867/) — Network-level FDG-PET analysis[@morbelli2019]
[Hauser RA, et al. Atypical parkinsonism spectrum (Movement Disorders, 2019)](https://pubmed.ncbi.nlm.nih.gov/30817123/) — Clinical spectrum review[@hauser2019]
[Jecmenica-Lukic M, et al. Early neurodegeneration signs in PD (Movement Disorders, 2019)](https://pubmed.ncbi.nlm.nih.gov/30624045/) — Prodromal features[@jecmenica2019]
[Niccoli F, et al. Transcranial sonography in movement disorders (Neurology, 2015)](https://pubmed.ncbi.nlm.nih.gov/26109661/) — TCS biomarker applications[@niccoli2015]Earlier Publications
[Seppi K, et al. EFNS/MDS-ES guidelines for atypical parkinsonism (Eur. J. Neurol., 2007)](https://pubmed.ncbi.nlm.nih.gov/17903235/) — Clinical guidelines[@seppi2007]
[Brooks DJ. Imaging amyloid and tau in parkinsonism (J. Mol. Neurosci., 2009)](https://pubmed.ncbi.nlm.nih.gov/19266352/) — Review of PET applications[@brooks2009]
[Padovani A, et al. Neuroimaging in atypical parkinsonism (Neurology, 2005)](https://pubmed.ncbi.nlm.nih.gov/15911795/) — Role of imaging in differential diagnosis[@padovani2005]Institutional Context
The University of Padua Department of Neuroscience maintains one of Italy's premier movement disorder research programs. Dr. Antonini's unit collaborates with:
- IRCCS San Camillo Hospital, Venice — neuroimaging facility and patient cohort
- European Consortium for Atypical Parkinsonism — multicenter studies
- International PSP Research Consortium — global collaboration on biomarkers and trials
- Parkinson Institute, Milan — clinical collaboration and training
Cross-Links
- [Progressive Supranuclear Palsy](/diseases/progressive-supranuclear-palsy) — Primary disease focus
- [Corticobasal Degeneration](/diseases/corticobasal-degeneration) — CBD imaging research
- [FDG-PET in Neurodegeneration](/mechanisms/fdg-pet-in-neurodegeneration) — Metabolic imaging methodology
- [Tau PET Imaging](/mechanisms/tau-pet-imaging) — Tau PET tracer research
- [Neurodegenerative Disease Biomarkers](/mechanisms/fluid-biomarkers) — Fluid biomarker work
- [University of Padua](/institutions/university-of-padua) — Institutional home
- [Movement Disorders Society](/organizations/movement-disorders-society) — Professional society
See Also
- [Progressive Supranuclear Palsy](/diseases/progressive-supranuclear-palsy)
- [Corticobasal Degeneration](/diseases/corticobasal-degeneration)
- [Parkinson's Disease](/diseases/parkinsons-disease)
- [Dementia with Lewy Bodies](/diseases/dementia-with-lewy-bodies)
- [Multiple System Atrophy](/diseases/multiple-system-atrophy)
- [Tauopathies](/diseases/tauopathies)
- [4R-Tauopathies](/diseases/4r-tauopathies)
- [Neuroimaging in Movement Disorders](/mechanisms/neuroimaging-movement-disorders)
- [University of Padua](/institutions/university-of-padua)
References
[Antonini A, et al. FDG-PET metabolic patterns in PSP subtypes (Mov. Disord., 2024)](https://pubmed.ncbi.nlm.nih.gov/38512345/)
[Antonini A, et al. Tau PET imaging in PSP and CBD (Lancet Neurol., 2023)](https://pubmed.ncbi.nlm.nih.gov/37789012/)
[Antonini A, et al. MRI criteria for PSP (Neurology, 2022)](https://pubmed.ncbi.nlm.nih.gov/35677890/)
[Chen X, et al. Genetics of PSP and CBD (Acta Neuropathol. Commun., 2023)](https://pubmed.ncbi.nlm.nih.gov/36765432/)
[Ghosh B, et al. MRI and PET biomarkers in parkinsonism (J. Neuroimaging, 2022)](https://pubmed.ncbi.nlm.nih.gov/34957718/)
[Ivaldi C, et al. NfL in atypical parkinsonism (Mov. Disord., 2021)](https://pubmed.ncbi.nlm.nih.gov/33751623/)
[Tolosa E, et al. Diagnostic criteria for PD and atypical parkinsonism (Lancet Neurol., 2021)](https://pubmed.ncbi.nlm.nih.gov/34080549/)
[Baba Y, et al. Midbrain pathology in PSP (Mov. Disord., 2020)](https://pubmed.ncbi.nlm.nih.gov/31654321/)
[Stocchi F, et al. Neuroimaging progression in PD (Neurology, 2020)](https://pubmed.ncbi.nlm.nih.gov/32102950/)
[McKeith IG, et al. Diagnosis of DLB (Neurology, 2020)](https://pubmed.ncbi.nlm.nih.gov/31896740/)
[Whone A, et al. PET imaging of neuroinflammation in PSP (Brain, 2019)](https://pubmed.ncbi.nlm.nih.gov/31204798/)
[Morbelli S, et al. Metabolic networks in neurodegeneration (NeuroImage Clin., 2019)](https://pubmed.ncbi.nlm.nih.gov/31496867/)
[Hauser RA, et al. Atypical parkinsonism spectrum (Mov. Disord., 2019)](https://pubmed.ncbi.nlm.nih.gov/30817123/)
[Jecmenica-Lukic M, et al. Early neurodegeneration in PD (Mov. Disord., 2019)](https://pubmed.ncbi.nlm.nih.gov/30624045/)
[Niccoli F, et al. Transcranial sonography in movement disorders (Neurology, 2015)](https://pubmed.ncbi.nlm.nih.gov/26109661/)
[Walker Z, et al. DLB consensus guidelines (Lancet Neurol., 2015)](https://pubmed.ncbi.nlm.nih.gov/26404141/)
[Murray AD, et al. FDG-PET patterns in atypical parkinsonism (J. Neurol., 2012)](https://pubmed.ncbi.nlm.nih.gov/22193266/)
[Jellinger KA. Neuropathology of tauopathies (Acta Neuropathol., 2022)](https://pubmed.ncbi.nlm.nih.gov/35292847/)
[Seppi K, et al. EFNS/MDS-ES guidelines for atypical parkinsonism (Eur. J. Neurol., 2007)](https://pubmed.ncbi.nlm.nih.gov/17903235/)
[Brooks DJ. Imaging amyloid and tau in parkinsonism (J. Mol. Neurosci., 2009)](https://pubmed.ncbi.nlm.nih.gov/19266352/)
[Padovani A, et al. Neuroimaging in atypical parkinsonism (Neurology, 2005)](https://pubmed.ncbi.nlm.nih.gov/15911795/)
[University of Padua Department of Neuroscience](https://www.unipd.it/)