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Long-Term Changes in Axon Calibers after Injury: Observations on the Mouse Corticospinal Tract
Athanasios S Alexandris1, Yiqing Wang1, Constantine E Frangakis2
1Department of Pathology, Johns Hopkins School of Medicine, Baltimore, MD 21205, USA.
International Journal of Molecular Sciences
|July 9, 2022
Summary
Traumatic brain injury alters axon diameter distribution in mice, with early loss of large axons and later changes suggesting functional adaptation. These changes can help distinguish injured from non-injured individuals.
Area of Science:
- Neuroscience
- Neuropathology
- Biomarker Development
Background:
- White matter pathology is prevalent in neurological diseases, necessitating better characterization for mechanistic understanding and biomarker discovery.
- Axon caliber is tightly regulated and changes in axon diameter distribution (ADD) are implicated in various neurological conditions and models.
- Traumatic brain injury (TBI) models offer a platform to study early and late white matter alterations.
Purpose of the Study:
- To investigate early and late changes in the axon diameter distribution (ADD) of the mouse corticospinal tract following impact acceleration-TBI (IA-TBI).
- To determine if ADD features can serve as reliable indicators for discriminating between injured and non-injured states.
- To explore the potential of ADD signatures for developing novel neuroimaging biomarkers for white matter pathology.
Main Methods:
- Utilized the impact acceleration model of traumatic brain injury (IA-TBI) in mice.
- Assessed changes in the axon diameter distribution (ADD) of the corticospinal tract using advanced Airyscan and electron microscopy techniques.
- Analyzed ADD parameters at early (day 7) and late (day 21) time points post-injury.
Main Results:
- Axon calibers in the corticospinal tract follow a lognormal distribution, with significant parameter changes post-IA-TBI.
- IA-TBI caused a 30% loss of corticospinal axons by day 7, preferentially affecting larger caliber axons.
- By day 21, a redistribution of axon frequencies was observed, characterized by a reduction in large-caliber axons without detectable degeneration, suggesting potential functional adaptation.
Conclusions:
- Changes in axon diameter distribution (ADD) following IA-TBI may represent functional adaptations in injured neural systems.
- ADD features demonstrate potential as accurate discriminators between injured and non-injured mice.
- Investigating ADD signatures through histology or advanced neuroimaging could lead to more nuanced characterization of white matter pathology and novel biomarker development.
