Back

Next Generation AAV-F Capsid gene therapy rescues disease pathology in a model of Pyruvate Dehydrogenase Complex Deficiency

Keegan, A.; Cetin, O.; Chilcott, E. M.; Antinao Diaz, J. F.; Eaton, S.; Waddington, S. N.; Counsell, J. R.; Rahman, S.; Karda, R.

2025-08-01 neuroscience
10.1101/2025.07.30.667478 bioRxiv
Show abstract

Pyruvate dehydrogenase complex deficiency (PDHD) is a severe mitochondrial disorder most frequently caused by pathogenic variants in PDHA1, leading to neurodevelopmental delay and early mortality, necessitating brain-targeted interventions. Using a brain-specific Pdha1 knockout mouse model, we compared intracerebroventricular delivery of AAV9 capsid and a recently described synthetic neurotropic AAV-F capsid, both expressing human PDHA1 coding sequence driven by a constitutive CAG promoter. Newborn mice received, titre matched AAV9 or AAV-F or AAV9 at ten-fold higher dose. Low-dose AAV-F and high-dose AAV9 significantly improved survival, and restored PDH enzyme activity, metabolite profiles, and brain histopathology to near wild-type levels. However, treated mice showed reduced locomotion by P100 and impaired motor function. Importantly, AAV-F achieved broad CNS transduction with minimal liver expression, outperforming AAV9 at lower dose. There results support the therapeutic potential of AAV-based gene therapy for PDHD and highlighting AAV-F as a promising capsid for efficient, CNS specific delivery.

Published in Molecular Therapy Advances · not in our set (fewer than 10 published preprints to learn from) · training set

Matching journals

The top 3 journals account for 50% of the predicted probability mass.

50% of probability mass above

"Similar papers" are the closest papers from that journal in the model's embedding space. They show what the match is built on, but the ranking comes mostly from a classifier over the whole training set, not from these examples alone.