Traumatic brain injury and amyloid-β pathology: a link to Alzheimer's disease?

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Abstract

Traumatic brain injury (TBI) has devastating acute effects and in many cases seems to initiate long-term neurodegeneration. Indeed, an epidemiological association between TBI and the development of Alzheimer's disease (AD) later in life has been demonstrated, and it has been shown that amyloid-β (Aβ) plaques — one of the hallmarks of AD — may be found in patients within hours following TBI. Here, we explore the mechanistic underpinnings of the link between TBI and AD, focusing on the hypothesis that rapid Aβ plaque formation may result from the accumulation of amyloid precursor protein in damaged axons and a disturbed balance between Aβ genesis and catabolism following TBI.

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Figure 1: Immunohistochemical findings exploring mechanisms of amyloid-β plaque formation following traumatic brain injury.
Figure 2: Potential mechanisms of post-traumatic amyloid-β formation and clearance.

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Acknowledgements

This work was supported by US National Institutes of Health grants NS038104 and NS056202.

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Correspondence to Douglas H. Smith.

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