Our approach leverages a convolutional neural network (CNN) architecture to automatically learn high-level representations from raw IMU signals, minimizing reliance on manual feature engineering. Central to our method is a two-stage training strategy that incorporates domain adversarial learning, enabling knowledge transfer between two IMU-based assessment tools: the Ataxia Instrumented Measures cup (AIM-C) and spoon (AIM-S). This strategy enhances learning from each device by exploiting shared underlying representations.
Wednesday, July 8, 2026
Domain Adaptation for IMU Data to Enhance Objective Assessment of Friedreich Ataxia
Tran, M., Ranaweera, K., Ngo, T., Pathirana, P., Milne, S., Horne, M., Delatycki, M., & Corben, L. (2026). Domain Adaptation for IMU Data to Enhance Objective Assessment of Friedreich Ataxia. IEEE Journal of Biomedical and Health Informatics, PP. doi:10.1109/JBHI.2026.3702417
Epigenetic reactivation in Friedreich’s ataxia from benzamides to gene‑targeted chimeras
Ansari, F. U., Rojsajjakul, T., Liu, J., Nageshwaran, S. K., & Blair, I. A. (2026). Epigenetic reactivation in Friedreich’s ataxia from benzamides to gene‑targeted chimeras. Expert Opinion on Drug Discovery, 21(7), 779–791. doi:10.1080/17460441.2026.2689723
This review summarizes the evolution of FXN protein‑reactivating approaches from first‑generation systemic epigenetic therapies, including class I‑selective benzamide histone deacetylase inhibitors and high‑dose nicotinamide, to emerging locus‑targeted platforms such as anti‑gene oligonucleotides and gene‑targeted chimera small molecules. The authors also examine splice‑modulating strategies aimed at increasing the extra‑mitochondrial FXN‑E isoform, discuss delivery and safety challenges across modalities, and highlight biomarker frameworks integrating isoform‑resolved FXN protein measurements and chromatin readouts.
Advances in Gene and Cellular Therapy in Friedreich Ataxia
Lazaropoulos MP, Lynch DR. Advances in Gene and Cellular Therapy in Friedreich Ataxia. Mol Diagn Ther. 2026 Jun 29. doi: 10.1007/s40291-026-00854-5. Epub ahead of print. PMID: 42373844.
Multiple investigational techniques and strategies seek to permanently alter the disease course in patients with Friedreich ataxia, although no product has established definitive benefit. This review catalogs both the history and ongoing efforts of genetic and cellular therapies applied to Friedreich ataxia and its disease models, including therapeutic efficacy and adverse effects. We list the key limitations and cautions of such therapies, chiefly those of potential FXN overexpression toxicity, critical therapeutic windows, and adverse effects of these therapies applicable to any disease target. As gene and cellular therapy continue to diversify in design and strategy, Friedreich ataxia patients will likely have multiple therapeutic options in the future from both investigational therapies described here and future ones yet to be optimized.
Frataxin attenuates endothelial inflammation triggered by engulfment of senescent erythrocytes
Hypertension is linked to a shortened erythrocyte lifespan, with endothelial cells acting as non-professional phagocytes to clear senescent erythrocytes. However, whether increased erythrophagocytosis contributes to endothelial inflammation remains unclear. Frataxin (FXN) plays a crucial role in controlling iron balance and metabolism. This study investigated the role of FXN-mediated iron engulfment in regulating endothelial pro-inflammatory phenotype.
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