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[11C]PK11195 PET in Alzheimer’s disease and progressive supranuclear palsy: the NIMROD study

P. Vazquez Rodriguez, J. Rowe, J. O'Brien, F. Aigbirhio, T. Fryer, L. Su, E. Mak, A. Surendranathan, R. Borchert, S. Jones, R. Arnold, R. Bevan-Jones, L. Passamonti, Y. Hong (Cambridge, United Kingdom)

Meeting: 2017 International Congress

Abstract Number: 169

Keywords: Microglial activation, Positron emission tomography(PET), Progressive supranuclear palsy(PSP)

Session Information

Date: Monday, June 5, 2017

Session Title: Parkinsonism, MSA, PSP (Secondary and Parkinsonism-Plus)

Session Time: 1:45pm-3:15pm

Location: Exhibit Hall C

Objective: Here we test whether the intensity and regional distribution of neuro-inflammation differs between Alzheimer’s disease (AD), Progressive Supranuclear Palsy (PSP) and controls; and whether neuro-inflammation relates to disease severity. 

Background: Neuro-inflammation plays a significant role in the pathogenesis of AD and PSP.

Methods: We used the radiotracer [11C]PK11195 with positron emission tomography and kinetic modeling to compare regional [11C]PK11195 binding in 16 patients with AD pathology (including amyloid-positive mild cognitive impairment), 16 with PSP, and 13 controls. We correlated [11C]PK11195 binding with clinical variables and C-reactive protein.

Results: [11C]PK11195 binding in the medial temporal lobe and occipital-parietal cortex was increased in AD patients, relative to both PSP patients and controls. PSP patients showed elevated [11C]PK11195 binding in the thalamus, putamen, and pallidum relative to controls. [11C]PK11195 binding in the pre-cuneus correlated negatively with episodic memory in AD, while [11C]PK11195 binding in the pallidum, midbrain, and pons correlated positively with disease severity in PSP.

Conclusions: The magnitude and distribution of neuro-inflammation, indexed by [11C]PK11195, differed between AD and PSP, and mirrored the established neuropathological distribution for each disease. In both AD and PSP, disease severity correlated with neuro-inflammation in the regions most closely associated with principal neuropathological markers including tau aggregates. Immunotherapeutic strategies targeting neuro-inflammation may be a useful strategy in slowing the progression of these neurodegenerative disorders.

References: Cagnin A, Brooks DJ, Kennedy AM, et al. In-vivo measurement of activated microglia in dementia. Lancet 2001;358(9280):461–467.  

Fernández-Botrán R, Ahmed Z, Crespo FA, et al. Cytokine expression and microglial activation in progressive supranuclear palsy. Parkinsonism Relat. Disord. 2011;17(9):683–688.

To cite this abstract in AMA style:

P. Vazquez Rodriguez, J. Rowe, J. O'Brien, F. Aigbirhio, T. Fryer, L. Su, E. Mak, A. Surendranathan, R. Borchert, S. Jones, R. Arnold, R. Bevan-Jones, L. Passamonti, Y. Hong. [11C]PK11195 PET in Alzheimer’s disease and progressive supranuclear palsy: the NIMROD study [abstract]. Mov Disord. 2017; 32 (suppl 2). https://www.mdsabstracts.org/abstract/11cpk11195-pet-in-alzheimers-disease-and-progressive-supranuclear-palsy-the-nimrod-study/. Accessed May 13, 2025.
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