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Comment
. 2018 Jul;28(4):463-465.
doi: 10.1111/bpa.12534.

Traumatic brain injury: a platform for studies in Aβ processing: Commentary on: "Rapid Aβ oligomer and protofibril accumulation in traumatic brain injury"

Douglas H Smith  1 , William Stewart  2
Affiliations
Comment

Traumatic brain injury: a platform for studies in Aβ processing: Commentary on: "Rapid Aβ oligomer and protofibril accumulation in traumatic brain injury"

Douglas H Smith et al. Brain Pathol. 2018 Jul.
No abstract available

Keywords: amyloid-beta; diffuse axonal injury; oligomers; protofilaments; traumatic brain injury.

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Figures

Figure 1
Figure 1
One potential source for rapid genesis of amyloid‐beta (Aβ) species after traumatic brain injury (TBI). A. Widespread damage to axons induces transport interruption and accumulation of amyloid precursor protein (APP) and the secretases, PS‐1 and BACE that can cleave it to form Aβ peptides within axonal swellings. B. Accumulating Aβ assembles into oligomers and protofibrils, that are (C) released into the brain when the axonal bulb is lysed. D. Free Aβ oligomers, protofibrils and developing fibrils may exert toxicity to the brain and/or form plaques that can be observed within hours after TBI.
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References

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