Assessment of a novel neuroinflammation radiotracer in cerebral small vessel disease
Motivation: Cerebral small vessel disease (cSVD) is a leading cause of vascular contributions to cognitive impairment & dementia ( VCID ). Understanding the relationship between neuroinflammation and cSVD using a novel radiotracer may enhance early diagnosis Goal(s): Investigate the specific binding of a PET radiotracer targeting the sphingosine 1-phosphate (S1P) receptor S1PR1 and its correlation with white matter hyperintensity (WMH) burden in cSVD Approach: Immunohistochemistry, Immunofluorescence, in vitro autoradiography (ARG), and blocking study using postmortem brain tissues to analyze S1PR1 expression and its association with WMH Results: Colocalization/correlation between S1PR1,astrocytes and microglia were observed. ARG revealed trend in white matter S1PR1 expression's association with WMH volumes Impact: Suggests a potential link between S1PR1 expression and neuroinflammation processes in cSVD and highlights the association with WMH burden. Provides preliminary evidence to support a new PET radiotracer targeting S1PR1 as an imaging biomarker to investigate neuroinflammation in cSVD
Authors
- Tammie L.S. Benzinger (ORCID: https://orcid.org/0000-0002-8114-0552)
- Andria L. Ford (ORCID: https://orcid.org/0000-0003-0605-8943)
- Inema Orukari
- Yasheng Chen (ORCID: https://orcid.org/0000-0002-1133-452X)
- Hongyu An (ORCID: https://orcid.org/0000-0001-6459-2269)
- Yujie Wang
- Bo Wang (ORCID: https://orcid.org/0000-0002-1192-0668)
- Jin-Moo Lee
- Hao Jiang (ORCID: https://orcid.org/0000-0002-8845-4378)
- Zhude Tu
Publication Details
- Journal
- Proceedings on CD-ROM - International Society for Magnetic Resonance in Medicine. Scientific Meeting and Exhibition/Proceedings of the International Society for Magnetic Resonance in Medicine, Scientific Meeting and Exhibition
- Published
- 2025-09-16
- DOI
- https://doi.org/10.58530/2025/3602
- Primary Topic
- Neurological Disease Mechanisms and Treatments
- Type
- article
- Field-Weighted Citation Impact
- 0.00