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Neurology. 2017 Aug 22;89(8):845-853. doi: 10.1212/WNL.0000000000004264. Epub 2017 Jul 28.

In vivo retention of 18F-AV-1451 in corticobasal syndrome.

Author information

1
From the Departments of Neurology (R.S., H.W., C.N.), Clinical Neurophysiology (D.H.), Radiation Physics (T.O.), and Clinical Physiology and Nuclear Medicine (J.J.), Skåne University Hospital (D.v.W.), Lund; Clinical Memory Research Unit (R.S., M.S., C.N., O.H.), Department of Clinical Sciences (D.v.W.), and Department of Diagnostic Radiology (D.v.W.), Lund University, Malmö; Wallenberg Centre for Molecular and Translational Medicine and the Department of Psychiatry and Neurochemistry (M.S.), University of Gothenburg; Department of Clinical Neuroscience (P.S.), CMM L8:01, Stockholm; and Memory Clinic (O.H.), Skåne University Hospital, Malmö, Sweden. Ruben.Smith@med.lu.se Oskar.Hansson@med.lu.se.
2
From the Departments of Neurology (R.S., H.W., C.N.), Clinical Neurophysiology (D.H.), Radiation Physics (T.O.), and Clinical Physiology and Nuclear Medicine (J.J.), Skåne University Hospital (D.v.W.), Lund; Clinical Memory Research Unit (R.S., M.S., C.N., O.H.), Department of Clinical Sciences (D.v.W.), and Department of Diagnostic Radiology (D.v.W.), Lund University, Malmö; Wallenberg Centre for Molecular and Translational Medicine and the Department of Psychiatry and Neurochemistry (M.S.), University of Gothenburg; Department of Clinical Neuroscience (P.S.), CMM L8:01, Stockholm; and Memory Clinic (O.H.), Skåne University Hospital, Malmö, Sweden.

Abstract

OBJECTIVE:

To study the usefulness of 18F-AV-1451 PET in patients with corticobasal syndrome (CBS).

METHODS:

We recruited 8 patients with CBS, 17 controls, 31 patients with Alzheimer disease (AD), and 11 patients with progressive supranuclear palsy (PSP) from the Swedish BioFINDER study. All patients underwent clinical assessment, 18F-AV-1451 PET, MRI, and quantification of β-amyloid pathology. A subset of participants also underwent 18F-FDG-PET.

RESULTS:

In the 8 patients with CBS, 6 had imaging findings compatible with the corticobasal degeneration pathology and 2 with typical AD pathology. In the 6 patients with CBS without typical AD pathology, there were substantial retentions of 18F-AV-1451 in the motor cortex, corticospinal tract, and basal ganglia contralateral to the most affected body side. These patients could be clearly distinguished from patients with AD dementia or PSP using 18F-AV-1451. However, cortical atrophy was more widespread than the cortical retention of 18F-AV1451 in these CBS cases, and cortical AV-1451 uptake did not correlate with cortical thickness or glucose hypometabolism. These results are in sharp contrast to AD dementia, where 18F-AV-1451 retention was more widespread than cortical atrophy, and correlated well with cortical thickness and hypometabolism.

CONCLUSIONS:

Patients with CBS without typical AD pathology exhibited AV-1451 retention in the motor cortex, corticospinal tract, and basal ganglia contralateral to the affected body side, clearly different from controls and patients with AD dementia or PSP. However, cortical atrophy measured with MRI and decreased 18F-fluorodeoxyglucose uptake were more widespread than 18F-AV-1451 uptake and probably represent earlier, yet less specific, markers of CBS.

CLASSIFICATION OF EVIDENCE:

This study provides Class III evidence that 18F-AV-1451 PET distinguishes between CBS and AD or PSP.

PMID:
28754841
PMCID:
PMC5580862
DOI:
10.1212/WNL.0000000000004264
[Indexed for MEDLINE]
Free PMC Article

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