Neurodegeneration
Can a new PET imaging tracer distinguish different tau diseases?
Open access · cc by · source: Europe PMC
A new brain scanning chemical successfully maps and tells apart two different types of degenerative brain disorders based on where protein tangles build up.
How this study connects
Role on claims
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Diagnostic separation and molecular specificity are different properties, and only the first was demonstrated.
A tau tracer separated two diseases with high accuracy while its binding target remained uncertain. 18F-AV-1451 PET distinguished Alzheimer's disease from progressive supranuclear palsy with 94.1% accuracy — cortical binding against midbrain and basal ganglia binding — yet post-mortem analysis complicated what the tracer binds.
Evidence for the claim as stated.
How close any of these markers is to clinical use differs by orders of magnitude, and the authors disagree with the framing more than with each other. Tau PET separates two diseases at 94.1% in a selected sample, while the Parkinson's model's mid-70s accuracy is explicitly not a standalone diagnostic test, and the glymphatic ALPS index is a diffusion proxy not shown to equal cerebrospinal fluid clearance.
Evidence for the claim as stated.
Open questions
Tensions this paper is part of
From concept pages' “where studies disagree.” Disagreement means the same question; scope means different assays, populations, or outcomes.
How close any of these markers is to clinical use differs by orders of magnitude, and the authors disagree with the framing more than with each other. Tau PET separates two diseases at 94.1% in a selected sample, while the Parkinson's model's mid-70s accuracy is explicitly not a standalone diagnostic test, and the glymphatic ALPS index is a diffusion proxy not shown to equal cerebrospinal fluid clearance.
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Can a new PET imaging tracer distinguish different tau diseases?
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19 patients with progressive supranuclear palsy
We recruited 19 patients with PSP [‘probable PSP’ by Movement Disorder Society criteria (, ), representing the ‘classical phenotype’, which is sometimes referred to as Richardson’s syndrome], nine patients meeting diagnostic criteria for probable Alzheimer’s disease (), and six patients with MCI and biomarker evidence of Alzheimer’s disease (i.e. amyloid pathology).
thirteen healthy controls
Thirteen age- and sex-matched healthy controls with no history of major psychiatric or neurological illnesses, head injury or any other significant medical co-morbidity were also included to allow group-wise comparisons with the clinical cohorts.
Key findings
The scans differentiated patients with Alzheimer's from those with progressive supranuclear palsy with 94.1% accuracy, showing high tracer binding in cortical regions for Alzheimer's and in the midbrain and basal ganglia for progressive supranuclear palsy. However, post-mortem analyses revealed that while the tracer bound specifically to the classic tau tangles of Alzheimer's, its binding in progressive supranuclear palsy and healthy control tissues was largely non-specific and off-target.
Methodology
The researchers scanned 19 patients with progressive supranuclear palsy, nine patients with Alzheimer's disease, six patients with mild cognitive impairment who had positive amyloid biomarker scans, and thirteen healthy controls using a PET tracer to map tau protein deposits in the brain. They also analyzed post-mortem brain tissues from three deceased donors—one with Alzheimer's, one with progressive supranuclear palsy, and one healthy control—to compare the scan results with physical brain samples.
Limitations
This study was cross-sectional, meaning it cannot demonstrate how the tracer's binding changes over time or how it would react to treatments. Furthermore, the findings are limited by the small sample sizes, particularly in the Alzheimer's and mild cognitive impairment groups. The study also could not identify the specific molecules causing the off-target tracer binding observed in the basal ganglia, which occurred even though post-mortem analysis showed no neuromelanin-containing cells there.
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