Department of Neurology, Massachusetts General Hospital, Boston, MA, USA.
Department of Neuroradiology, Heidelberg University, Heidelberg, Germany.
Nat Commun. 2023 Apr 5;14(1):1900. doi: 10.1038/s41467-023-37262-w.
Blood-brain barrier disruption marks the onset of cerebral adrenoleukodystrophy (CALD), a devastating cerebral demyelinating disease caused by loss of ABCD1 gene function. The underlying mechanism are not well understood, but evidence suggests that microvascular dysfunction is involved. We analyzed cerebral perfusion imaging in boys with CALD treated with autologous hematopoietic stem-cells transduced with the Lenti-D lentiviral vector that contains ABCD1 cDNA as part of a single group, open-label phase 2-3 safety and efficacy study (NCT01896102) and patients treated with allogeneic hematopoietic stem cell transplantation. We found widespread and sustained normalization of white matter permeability and microvascular flow. We demonstrate that ABCD1 functional bone marrow-derived cells can engraft in the cerebral vascular and perivascular space. Inverse correlation between gene dosage and lesion growth suggests that corrected cells contribute long-term to remodeling of brain microvascular function. Further studies are needed to explore the longevity of these effects.
血脑屏障破坏标志着脑肾上腺脑白质营养不良(CALD)的发作,这是一种由 ABCD1 基因功能丧失引起的毁灭性脑脱髓鞘疾病。其潜在机制尚不清楚,但有证据表明微血管功能障碍与之相关。我们分析了接受含有 ABCD1 cDNA 的 Lenti-D 慢病毒载体转导的自体造血干细胞治疗的 CALD 男孩的脑灌注成像,这些男孩是作为单一组参与开放性、2-3 期安全性和疗效研究(NCT01896102)的患者,以及接受异基因造血干细胞移植的患者。我们发现白质通透性和微血管血流广泛且持续正常化。我们证明 ABCD1 功能正常的骨髓源性细胞可以在脑血管和血管周围空间中定植。基因剂量与病变生长之间的反比关系表明,纠正后的细胞长期有助于脑微血管功能的重塑。需要进一步研究来探索这些效果的持久性。