A pilot [11C]PBR28 PET/MRI study of neuroinflammation and neurodegeneration in chronic stroke patients

Judith D. Schaechter; Baileigh G. Hightower; Minhae Kim; Marco L. Loggia

Brain, Behavior, & Immunity - Health (Nov 2021)

A pilot [11C]PBR28 PET/MRI study of neuroinflammation and neurodegeneration in chronic stroke patients

Judith D. Schaechter,
Baileigh G. Hightower,
Minhae Kim,
Marco L. Loggia

Affiliations

Judith D. Schaechter: Corresponding author.; Athinoula A. Martinos Center for Biomedical Imaging Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 13th Street, Building 149, Room 2301, Charlestown, MA, 02129, USA
Baileigh G. Hightower: Athinoula A. Martinos Center for Biomedical Imaging Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 13th Street, Building 149, Room 2301, Charlestown, MA, 02129, USA
Minhae Kim: Athinoula A. Martinos Center for Biomedical Imaging Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 13th Street, Building 149, Room 2301, Charlestown, MA, 02129, USA
Marco L. Loggia: Athinoula A. Martinos Center for Biomedical Imaging Department of Radiology, Massachusetts General Hospital, Harvard Medical School, 13th Street, Building 149, Room 2301, Charlestown, MA, 02129, USA

Journal volume & issue: Vol. 17
p. 100336

Abstract

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Neuroinflammation occurs in response to acute ischemic stroke, and has been speculated to underlie secondary poststroke pathologies, such as depression, that often develop over time poststroke. However, no study has examined whether neuroinflammation is present in chronic stroke patients (e.g., ≥ 1 year poststroke). This study tested whether neuroinflammation is present in chronic stroke patients, and is associated with neurodegeneration, using [11C]PBR28 PET and diffusion MRI.Eight patients with middle cerebral artery (MCA) ischemic stroke incurred 1–3 years prior and 16 healthy controls underwent [11C]PBR28 PET to measure glial activation and diffusion MRI to measure microstructural integrity by mean diffusivity (MD) and fractional anisotropy (FA) using an integrated PET/MRI scanner. Group differences in [11C]PBR28 binding, MD and FA were analyzed voxelwise across the whole brain excluding the infarct zone defined as voxels containing the infarct in any patient.Compared to controls, patients showed elevations in [11C]PBR28 binding in several brain regions outside the infarct zone, including regions with presumed direct neuroanatomical connections to the infarct (e.g., ipsilesional internal capsule and thalamus) and those without known direct connections (e.g., contralesional thalamus and cingulate gyrus). Patients also showed widespread elevations in MD, with a subset of these regions having reduced FA. In patients, MD was more elevated in regions with co-localized elevations in [11C]PBR28 binding than in contralateral regions without elevations in [11C]PBR28 binding.This pilot study supports the presence of extensive glial activation along with widespread loss in microstructural integrity in non-infarcted tissue in a cohort of patients with chronic MCA stroke. The loss in microstructural integrity was greater in regions with co-localized glial activation. It is possible that stroke risk factors (e.g., hypertension) contributed to these tissue changes in patients.

Published in Brain, Behavior, & Immunity - Health

ISSN: 2666-3546 (Online)
Publisher: Elsevier
Country of publisher: United States
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.journals.elsevier.com/brain-behavior-and-immunity-health

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