Traumatic Brain Injury Model
Objective: To induce and characterize traumatic brain injury in mice to assess glymphatic pathway dysfunction and tau pathology development
This is a Traumatic Brain Injury Model protocol using mouse as the model organism. The procedure involves 5 procedural steps. Extracted from a 2014 paper published in Journal of Neuroscience.
Model and subjects
mouse • Not explicitly stated in provided text • unknown • Not explicitly stated in provided text • Not explicitly stated in provided text
Study window
Estimated timing pending
Core workflow
Traumatic Brain Injury Induction • Assess Glymphatic Pathway Function • Evaluate Tau Clearance
Primary readouts
- Glymphatic pathway function reduction (approximately 60% impairment)
- Duration of glymphatic pathway impairment (at least 1 month post-injury)
- Extracellular tau clearance from brain
- Development of neurofibrillary tangles and tau aggregates
Key equipment and reagents
Verified items
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Direct vendor links
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Protocol Steps
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Traumatic Brain Injury Induction
Induce traumatic brain injury in mice using an unspecified method
Note: The specific TBI induction method is not detailed in the provided text excerpt
View evidence from paper
“After TBI, glymphatic pathway function was reduced by ∼60%, with this impairment persisting for at least 1 month post injury”
Assess Glymphatic Pathway Function
Measure glymphatic pathway function post-injury to quantify impairment
Note: Glymphatic pathway function was reduced by approximately 60% after TBI
View evidence from paper
“After TBI, glymphatic pathway function was reduced by ∼60%, with this impairment persisting for at least 1 month post injury”
Evaluate Tau Clearance
Demonstrate that extracellular tau is cleared from the brain along paravascular pathways
Note: Tau clearance occurs via the glymphatic pathway
View evidence from paper
“Here we demonstrate in mice that extracellular tau is cleared from the brain along these paravascular pathways”
Assess Neurofibrillary Pathology Development
Evaluate development of neurofibrillary tangles and tau aggregation in post-traumatic brain
Note: Genetic knock-out of aquaporin-4 exacerbated pathology development
View evidence from paper
“Genetic knock-out of the gene encoding the astroglial water channel aquaporin-4, which is importantly involved in paravascular interstitial solute clearance, exacerbated glymphatic pathway dysfunction after TBI and promoted the development of neurofibrillary pathology”
Assess Neurodegeneration
Evaluate neurodegeneration in the post-traumatic brain
Note: Neurodegeneration was promoted in aquaporin-4 knockout mice
View evidence from paper
“exacerbated glymphatic pathway dysfunction after TBI and promoted the development of neurofibrillary pathology and neurodegeneration in the post-traumatic brain”