Zürcher, Nicole R.Loggia, MarcoLawson, RobertChonde, Daniel B.Izquierdo-Garcia, DavidYasek, Julia E.Akeju, OluwaseunCatana, CiprianRosen, BruceCudkowicz, MeritHooker, JacobAtassi, Nazem2015-03-022015Zürcher, N. R., M. L. Loggia, R. Lawson, D. B. Chonde, D. Izquierdo-Garcia, J. E. Yasek, O. Akeju, et al. 2015. “Increased in vivo glial activation in patients with amyotrophic lateral sclerosis: Assessed with [11C]-PBR28.” NeuroImage : Clinical 7 (1): 409-414. doi:10.1016/j.nicl.2015.01.009. http://dx.doi.org/10.1016/j.nicl.2015.01.009.2213-1582http://nrs.harvard.edu/urn-3:HUL.InstRepos:14065310Evidence from human post mortem, in vivo and animal model studies implicates the neuroimmune system and activated microglia in the pathology of amyotrophic lateral sclerosis. The study aim was to further evaluate in vivo neuroinflammation in individuals with amyotrophic lateral sclerosis using [11C]-PBR28 positron emission tomography. Ten patients with amyotrophic lateral sclerosis (seven males, three females, 38–68 years) and ten age- and [11C]-PBR28 binding affinity-matched healthy volunteers (six males, four females, 33–65 years) completed a positron emission tomography scan. Standardized uptake values were calculated from 60 to 90 min post-injection and normalized to whole brain mean. Voxel-wise analysis showed increased binding in the motor cortices and corticospinal tracts in patients with amyotrophic lateral sclerosis compared to healthy controls (pFWE < 0.05). Region of interest analysis revealed increased [11C]-PBR28 binding in the precentral gyrus in patients (normalized standardized uptake value = 1.15) compared to controls (1.03, p < 0.05). In patients those values were positively correlated with upper motor neuron burden scores (r = 0.69, p < 0.05), and negatively correlated with the amyotrophic lateral sclerosis functional rating scale (r = –0.66, p < 0.05). Increased in vivo glial activation in motor cortices, that correlates with phenotype, complements previous histopathological reports. Further studies will determine the role of [11C]-PBR28 as a marker of treatments that target neuroinflammation.en-USAmyotrophic lateral sclerosisPositron emission tomography[NeuroinflammationMicrogliaMotor cortexALS, amyotrophic lateral sclerosisALSFRS-R, amyotrophic lateral sclerosis functional rating scale revisedFWE, family-wise error rateMR, magnetic resonancePBR-28, peripheral benzodiazepine receptor 28PET, positron emission tomographySUV, standardized uptake valueTSPO, 18 kDa translocator proteinUMNB, upper motor neuron burden scaleVC, vital capacity.Journal Article2015-03-0210.1016/j.nicl.2015.01.009