Neuroinflammation and tau co‐localize in vivo in progressive supranuclear palsy

Publication: Annals of Neurology

Maura Malpetti, Luca Passamonti, Timothy Rittman, P. Simon Jones, Patricia Vázquez Rodríguez, W. Richard Bevan‐Jones, Young T. Hong, Tim D. Fryer, Franklin I. Aigbirhio, John T. O’Brien, James B. Rowe

20 September 2020


The researchers examined the relationship between tau pathology and neuroinflammation using [11C]PK11195 and [18F]AV‐1451 PET in 17 patients with progressive supranuclear palsy (PSP) Richardson’s syndrome. They tested the hypothesis that neuroinflammation and tau protein aggregation colocalize macroscopically, and correlate with clinical severity.

Regional [11C]PK11195 and [18F]AV‐1451 binding were positively correlated (R = 0.577, p < 0.0001). The PCA identified 4 components for each ligand, reflecting the relative expression of tau pathology or neuroinflammation in distinct groups of brain regions. Positive associations between [11C]PK11195 and [18F]AV‐1451 components’ loadings were found in both subcortical (R = 0.769, p < 0.0001) and cortical regions (R = 0.836, p < 0.0001). There were positive correlations between clinical severity and both subcortical tau pathology (R = 0.667, p = 0.003) and neuroinflammation (R = 0.788, p < 0.001).

The researchers show that tau pathology and neuroinflammation colocalize in PSP, and that individual differences in subcortical tau pathology and neuroinflammation are linked to clinical severity. Although longitudinal studies are needed to determine causal associations between these molecular pathologies, they suggest that the combination of tau‐ and immune‐oriented strategies may be useful for effective disease‐modifying treatments in PSP

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