18F-MK-6240 uptake in cortical tau and hemorrhagic lesions in a case of Alzheimer’s disease with possible crossed aphasia

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We report neuroimaging findings from a 74-year-old right-handed male with Alzheimer’s disease (AD) and lesions of cerebral amyloid angiopathy (CAA), utilizing 11 C-PiB-PET, 18 F-THK5351-PET, and 18 F-MK-6240-PET. 11 C-PiB-PET showed positive findings consistent with AD. 18 F-THK5351 accumulated in regions of astrogliosis due to tau pathology, subcortical hemorrhage, cortical superficial siderosis (cSS), and monoamine oxidase-B rich areas. 18 F-MK-6240 accumulated in regions with tau pathology, subcortical hemorrhage, and cSS, but not notably in CAA-related microbleeds (CMBs). 99m Tc-ECD SPECT, conducted 9 years post-diagnosis, revealed reduced cerebral blood flow in the bilateral lower temporal lobes and the right posterior temporo-parietal lobes, overlapping the subcortical hemorrhage and cSS. The patient exhibited progression of global cognitive decline and persistent word fluency deficits (name listing) on neuropsychological examination from the early stage of the disease, irrespective of the right hemorrhagic lesions in the non-dominant hemisphere, suggesting possible crossed aphasia. This is the first report of 18 F-MK-6240 binding to a subcortical hemorrhage and cSS lesions, highlighting its binding differences compared to smaller vascular leakages, such as CMBs due to CAA. These results may help refine PET imaging interpretation and diagnostic accuracy for AD with concurrent CAA. • 18 F-MK6240 accumulated in tau, subcortical hemorrhage, and superficial siderosis. • No uptake was observed in cerebral microbleeds. • This case exhibited progression of cognitive decline with possibly crossed aphasia.

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