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Estrogen Sulfotransferase-Mediated Imaging with Positron Emission Tomography in Moyamoya Syndrome

  • Author(s): Surmak, Andrew John
  • Advisor(s): Barrio, Jorge R.
  • et al.

Moyamoya syndrome presents a cerebrovascular pathology that progressively introduces chronic ischemia. The network of collateral vessels created in response to arterial stenosis causes hypoperfusion and stimulates inflammatory insults that jeopardize the brain. Within this study, we used positron emission tomography (PET) to image inflammatory responses in patients with moyamoya syndrome and present the first report of [11C]-PiB in moyamoya patients. [11C]-PiB has a high affinity for estrogen sulfotransferase (SULT1E1), which is a metabolic enzyme for estrogen that varies with inflammation. We used an animal model to verify whether SULT1E1 corresponded to [11C]-PiB signal. As moyamoya syndrome is susceptible to chronic ischemia, we hypothesized that resulting insults in tissue would present inflammatory responses that would cause SULT1E1 to be elevated. In addition to moyamoya patients, we also included a patient with multiple sclerosis (MS) for scanning before and after immunomodulatory therapy to verify whether changes in inflammation could be seen with therapy. [11C]-PiB produced a dynamic signal in response to inflammatory insults. In the animal model, the [11C]-PiB signal was localized with dense SULT1E1 immunohistochemistry stains in the peri-infarct area not seen on the contralateral side. [11C]-PiB SRTM DVR was markedly increased in the thalamus, pons, corona radiata and internal capsule of moyamoya patients when compared to controls (p<0.01). The MS patient had vast reduction in signal after one month of therapy that even achieved a 34% reduction in the right ventral pallidum. Collectively, these observations establish that [11C]-PiB signal reflects heightened inflammatory responses from SULT1E1. A� imaging with [11C]-PiB is not a signal achieved in this report. Neither MS nor moyamoya involve amyloid-beta (A�) as consequences of their progression. Therefore, the results in this report reflect [11C]-PiB signal as a consequence of fluctuating inflammatory responses in diseases that lack A�.

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