Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury

Acute axon damage and demyelination are mitigated by 4-aminopyridine (4-AP) therapy after experimental traumatic brain injury

Damage to long axons in white matter tracts is a major pathology in closed head traumatic brain injury (TBI). Acute TBI treatments are needed that protect against axon damage and promote recovery of axon function to prevent long term symptoms and neurodegeneration. Our prior characterization of axon...

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Bibliographic Details
Main Authors: Armstrong, R.C (Author), Galdzicki, Z. (Author), Lischka, F.W (Author), Noble, M.D (Author), Radomski, K.L (Author), Zi, X. (Author)
Format: Article
Language:English
Published: BioMed Central Ltd 2022
Subjects:
4-aminopyridine
4-Aminopyridine
animal
Animals
axon
Axons
Brain Injuries, Traumatic
C57BL mouse
controlled study
Demyelination
Electrophysiology
fampridine
female
Female
human
Humans
Kv1.2
male
Male
Mice
Mice, Inbred C57BL
mouse
multiple sclerosis
Multiple Sclerosis
pathology
randomized controlled trial
traumatic brain injury
Traumatic brain injury
White matter
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