ArticleBrain : a journal of neurology2026
Autologous adipose-derived mesenchymal stromal cells for chronic traumatic brain injury.
Article in Brain : a journal of neurology, 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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The abstract states no effect estimate the extractor could read, or names no intervention and outcome on the map, so this paper lights no cell and moves no belief. It is still indexed, cited and linked below.
The trial behind it
Trials whose registry record cites this paper, or whose number appears in the abstract. A trial that started after this paper was published is citing it as background, not reporting it.
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Who cites it
1 citing paper in PubMed.
- Future Directions and Evolution Strategies for the Clinical Management of Traumatic Brain Injury.Journal of clinical medicine · 2026Article
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Authors and funding
15 authors.
Funding
Abstract
Secondary injury from traumatic brain injury (TBI) leads to a chronic inflammatory process, neurodegeneration, and tissue loss, resulting in poor outcomes. Mesenchymal stromal cell (MSC) treatment can dampen microglial activation and improve TBI outcomes. Our study aimed to assess the impact of autologous adipose-derived MSC treatment in adult patients with chronic TBI using imaging, functional, and neurocognitive outcome measures. Our Phase 1/2a study analyzed safety and treatment effect of 3 intravenous infusions (over 6 weeks) of autologous adipose-derived MSCs (HB-adMSCs) in 24 chronic TBI patients. Outcome measures included functional, neuropsychological, and psychometric testing; multimodal MRI; and PET using [11C]ER176 to measure brain immune cell density. There were no serious treatment-related adverse events. DT-MRI analyses in a priori regions of interest showed that at 6 months after treatment, elevated mean diffusivity volumes (supraMD) were significantly reduced bilaterally in the hippocampus (mean decrease 163.51 mm3, 95% CI -286.55 to -41.51 mm3; P=0.013). A trend for reduced supraMD was observed in the amygdala (mean decrease 113.60 mm3, 95% CI -229.52 to 2.90 mm3; P=0.058); no changes in the insula were observed (P=0.19). Brain-behavior analyses indicated significant interactions between levels in baseline neuropsychological assessments of anxiety and depression and magnitude of supraMD changes in the amygdala and hippocampus, respectively. Macrostructural volumetric changes were not significant in the hippocampus, amygdala, or insula (all P >0.10). PET results showed that HB-adMSC treatment induced significant reductions in brain immune cell density in the right caudate (x,y,z: 12,2,7; T20 = 4.1; P <0.0003), extending into both the right ventral anterior thalamus (x,y,z: 13, -2,11; T20 = 3.6; P < 0.0009) and right nucleus accumbens (x,y,z: 8,9, -3; T20 = 2.5; P < 0.01), and right parahippocampal gyrus (x,y,z: 29, -40, -7; T20 = 3.1; P <0.003). Reductions in measures of depression (P=0.026), fatigue (P=0.008), and pain (P=0.007) 6 months after treatment were also observed. Our study demonstrates autologous adipose-derived MSCs for chronic TBI are safe, have clinically relevant treatment effect sizes in functional and neurocognitive outcome measures, yield significant improvements in specified measures of microstructural integrity (i.e., reduced volume of elevated MD voxels) in brain-based behavior relations, and reduce density of brain immune cells in regions corresponding to pain, fatigue, and depression. These data provide quantitative justification for the sample size of next-phase clinical trials using either functional outcomes or surrogate imaging outcomes.
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