Research Associate Professor
BSc, MSc, PhD
As Principal Investigator of The Neurology of Myopathies (NoM) Lab, Associate Professor Lindsay and his team conducts preclinical research focused on developing pharmaceutical and gene editing therapies for neuromuscular diseases, with a primary emphasis on muscular dystrophies, particularly Duchenne.
The NoM Lab’s work spans a broad spectrum of fundamental and translational biology, integrating physiology, neurology, behaviour, molecular biology, biochemistry, bio-imaging, and biomechanics.
Key research priorities include developing innovative therapeutics to stabilise skeletal muscle, uncovering mechanisms underlying neurological dysfunction, refining treatment dosing strategies, and advancing evaluation techniques to accelerate translation from preclinical studies to clinical application.
The NoM Lab has research collaborations across New Zealand and with international programs in Australia, France, Singapore, UK and the USA. Associate Professor Lindsay also facilitates and consults on therapeutic advancement to help bring clinical trials to New Zealand, ensuring patients have access to globally advanced treatments.
Beyond the science, the NoM Lab is committed to patient advocacy and community engagement through partnerships with organisations in New Zealand and internationally.
Current roles
- Research Associate Professor in Medicine
- Principal Investigator of the Neurology of Myopathies (NoM) Lab
- Scientific Advisor for the Muscular Dystrophy Association of New Zealand
- Neuromuscular Research Foundation Trust Chairperson
Positions and memberships
- Rare disorders researchers’ network – Rare Disorders New Zealand
- World Muscle Society
- Australasian Neuromuscular Network
- New Zealand Physiological Society
Publications
Major, G. S., Chen, J., van den Berg, E., Merry, D. L., & Lindsay, A. (2026). Regimen-dependent glucocorticoid effects improve muscle performance without altering CNS physiology in mdx mice. Journal of Physiology. Advance online publication. doi: 10.1113/jp291378 Journal - Research Article
Merry, D. L., Devananthan, P., Kabaliuk, N., & Lindsay, A. (2026). Viscoelastic properties of dystrophin-deficient mouse skeletal muscles are resilient to isometric fatiguing exercise. Physiological Reports, 14(6), e70841. doi: 10.14814/phy2.70841 Journal - Research Article
Devananthan, P., Craven, R., Joe, K., Major, G. S., Chen, J., Kabaliuk, N., & Lindsay, A. (2026). Dystrophin-deficiency stiffens skeletal muscle and impairs elasticity: An in vivo rheological examination. Journal of Applied Physiology, 140, 39-56. doi: 10.1152/japplphysiol.00492.2025 Journal - Research Article
Chen, M., Kimberley, T. J., Stark, M. M., Lindsay, A., Lowe, D. A., & Trost, J. P. (2025). Role of skeletal muscle excitability in strength loss induced by submaximal isometric contractions in males with Duchenne muscular dystrophy. Neuromuscular Disorders, 56-57, 106217. doi: 10.1016/j.nmd.2025.106217 Journal - Research Article
Major, G. S., Timpani, C. A., Russell, A. P., Rybalka, E., & Lindsay, A. (2025). Considering the potential of ovarian hormones in rescuing neurological phenotypes in Duchenne muscular dystrophy: It's time to think beyond the muscles. Medical Hypotheses, 204, 111766. doi: 10.1016/j.mehy.2025.111766 Journal - Research Article