Kiarra Ning
Current Organizations / Institutes
The organizations/institutes from the scholar's latest article
Research Subjects
Kiarra Ning has a total of 31 co-authors. Here are the top co-authors by number of shared publications:
- Ahmed Abdelhak
Department of Neurology and Weill Institute for Neurosciences University of California San Francisco CA USA
2 shared publications - Bruce Anthony Campbell Cree
Department of Neurology, UCSF Weill Institute for Neurosciences, University of California San Francisco, San Francisco, CA, USA
2 shared publications - Christian Cordano
Department of Neurology, Weill Institute for Neurosciences, University of California at San Francisco, San Francisco, USA
2 shared publications - Adam Santaniello
Department of Neurology, Weill Institute for Neurosciences, University of California, San Francisco
1 shared publication Adil Harroud
The Neuro (Montreal Neurological Institute-Hospital), Montreal, Canada
1 shared publication- Alexander Stahmann
MS Forschungs- und Projektentwicklungs-gGmbH, Germany
1 shared publication
Latest Publications
- Open Access
- 12 September 2026
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 115, 107914
Physiotherapy and confirmed disability improvement in people with multiple sclerosis
- 12 September 2026
- Published by Elsevier in Multiple Sclerosis and Related Disorders
- Vol. 115, 107914
Open AccessPhysiotherapy and confirmed disability improvement in people with multiple sclerosis
- Top Cited Papers
- 20 October 2025
- Published by Springer Nature in Nature Medicine
- Vol. 32 (1) , 362-368
Myelin injury precedes axonal injury and symptomatic onset in multiple sclerosis
The timing of the biological onset of multiple sclerosis (MS) is unclear. We used high-throughput discovery proteomics and samples from presymptomatic patients with MS and matched healthy controls to define the biological neurological onset and characterize the mechanisms involved. Remarkably, evidence of myelin injury was seen ~7 years before the symptomatic onset and preceded evidence of axonal injury by ~1 year. By contrast, astrocyte involvement became evident only at clinical onset. Numerous changes in the serum proteome indicate the involvement of interleukin 3 and nuclear factor kappa B pathways during the presymptomatic stage. Furthermore, people with MS with a previously reported distinct autoantibody signature showed increased immune cell activity compared to those without. We propose a protein biomarker panel that may help distinguish presymptomatic patients with MS from healthy controls, pending validation in future studies. Our findings can help understand the pathophysiology of MS as well as the cascade of central nervous system injury and might facilitate early detection of MS in high-risk people.
- 20 October 2025
- Published by Springer Nature in Nature Medicine
- Vol. 32 (1) , 362-368
Top Cited PapersMyelin injury precedes axonal injury and symptomatic onset in multiple sclerosis
The timing of the biological onset of multiple sclerosis (MS) is unclear. We used high-throughput discovery proteomics and samples from presymptomatic patients with MS and matched healthy controls to define the biological neurological onset and characterize the mechanisms involved. Remarkably, evidence of myelin injury was seen ~7 years before the symptomatic onset and preceded evidence of axonal injury by ~1 year. By contrast, astrocyte involvement became evident only at clinical onset. Numerous changes in the serum proteome indicate the involvement of interleukin 3 and nuclear factor kappa B pathways during the presymptomatic stage. Furthermore, people with MS with a previously reported distinct autoantibody signature showed increased immune cell activity compared to those without. We propose a protein biomarker panel that may help distinguish presymptomatic patients with MS from healthy controls, pending validation in future studies. Our findings can help understand the pathophysiology of MS as well as the cascade of central nervous system injury and might facilitate early detection of MS in high-risk people.