Douglas Smith and his colleagues at the University of Pennsylvania may have filled a gap in research on long-term, neurodegeneration sequelae of brain injuries by showing Aβ and tau production in an animal model of brain trauma. Their porcine model goes beyond previous rodent models, in which amyloid precursor protein (APP) but not Aβ production had been seen.

In their article in the current Journal of Neuropathology and Experimental Neurology, the researchers describe the effects of an experimental head injury model called rotational acceleration, which does not involve impact, but replicates a brain trauma commonly seen in car accidents. The 110-degree acceleration of the pig's head over 20 milliseconds produces diffuse brain injury, especially widespread axonal injury in the white matter.

Histopathology at three, seven, and 10 days following the trauma revealed Aβ and tau co-localized with APP and neurofilament proteins in damaged axons throughout the white matter. In about a third of the animals—those with the highest total amount of axonal pathology—Smith and his colleagues also found Aβ-containing plaques-like profiles in gray and white matter, as well as accumulations of tau and neurofilament-rich inclusions (similar to Lewy bodies) within cell bodies.—Hakon Heimer


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  1. . Accumulation of amyloid beta and tau and the formation of neurofilament inclusions following diffuse brain injury in the pig. J Neuropathol Exp Neurol. 1999 Sep;58(9):982-92. PubMed.