Brain architecture-based vulnerability to traumatic injury

The white matter tracts forming the intricate wiring of the brain are subject-specific; this heterogeneity can complicate studies of brain function and disease. Here we collapse tractography data from the Human Connectome Project (HCP) into structural connectivity (SC) matrices and identify groups o...

Full description

Saved in:
Bibliographic Details
Published inFrontiers in bioengineering and biotechnology Vol. 10; p. 936082
Main Authors Rifkin, Jared A., Wu, Taotao, Rayfield, Adam C., Anderson, Erin D., Panzer, Matthew B., Meaney, David F.
Format Journal Article
LanguageEnglish
Published Frontiers Media S.A 24.08.2022
Subjects
Online AccessGet full text

Cover

Loading…
More Information
Summary:The white matter tracts forming the intricate wiring of the brain are subject-specific; this heterogeneity can complicate studies of brain function and disease. Here we collapse tractography data from the Human Connectome Project (HCP) into structural connectivity (SC) matrices and identify groups of similarly wired brains from both sexes. To characterize the significance of these architectural groupings, we examined how similarly wired brains led to distinct groupings of neural activity dynamics estimated with Kuramoto oscillator models (KMs). We then lesioned our networks to simulate traumatic brain injury (TBI) and finally we tested whether these distinct architecture groups’ dynamics exhibited differing responses to simulated TBI. At each of these levels we found that brain structure, simulated dynamics, and injury susceptibility were all related to brain grouping. We found four primary brain architecture groupings (two male and two female), with similar architectures appearing across both sexes. Among these groupings of brain structure, two architecture types were significantly more vulnerable than the remaining two architecture types to lesions. These groups suggest that mesoscale brain architecture types exist, and these architectural differences may contribute to differential risks to TBI and clinical outcomes across the population.
Bibliography:ObjectType-Article-1
SourceType-Scholarly Journals-1
ObjectType-Feature-2
content type line 23
Spase Petkoski, INSERM U1106 Institut de Neurosciences des Systèmes, France
Edited by: Joel Douglas Stitzel, Wake Forest School of Medicine, United States
This article was submitted to Biomechanics, a section of the journal Frontiers in Bioengineering and Biotechnology
Reviewed by: Saber Jafarpour, Georgia Institute of Technology, United States
ISSN:2296-4185
2296-4185
DOI:10.3389/fbioe.2022.936082