Table 1.
Model | Time after injury | Pathology present | Reference |
---|---|---|---|
Rotational acceleration | 1 day | Increased gliosis in sulci accompanied by axonal swelling. | Smith et al., 1999a |
Fluid percussion injury | 24 h | Subarachnoid hemorrhage around area of impact. Aβ-positive neurons and axonal damage in white matter. Shrunken neurons and evidence of necrosis. | Fritz et al., 2005 |
Controlled cortical impact | 10 h | Perivascular hemorrhage around injury site. Damage to dendrites and decreased MAP2 staining. Fluro-Jade B-positive neurons mainly present in cell bodies, dendrites, and axons. | Manley et al., 2006 |
Rotational acceleration | 6 h | Increased subarachnoid bleeding in moderate accelerated pigs. APP accumulation and axonal injury in diencephalon region. No changes in NF68. | Ibrahim et al., 2010 |
Rotational accelerations | 6 h | Accumulation of Aβ and hyperphosphorylated tau in subcortical white matter. | Eucker et al., 2011 |
Rotational acceleration | 6 and 48–72 h | Initial APP accumulation post-injury in the periventricular white matter. Development of neurofibrillary subtypes in subcortical white matter. | Johnson et al., 2016 |
Rotational acceleration | 7 days | Electrophysiological recordings from CA1 field showed greater output. No accumulation of Aβ or hyperphosphorylated tau. | Wolf et al., 2017 |
Rotational acceleration | 6 and 48 h | Blood brain barrier leakage after concussion. Axonal swelling and beading. BBB leakage overlapped with APP-positive-labeled axons in white matter. | Johnson et al., 2018 |