A Lack of Amyloid β Plaques Despite Persistent Accumulation of Amyloid β in Axons of Long-Term Survivors of Traumatic Brain Injury
Article first published online: 19 MAY 2008
© 2008 The Authors. Journal Compilation © 2008 International Society of Neuropathology
Volume 19, Issue 2, pages 214–223, April 2009
How to Cite
Chen, X.-H., Johnson, V. E., Uryu, K., Trojanowski, J. Q. and Smith, D. H. (2009), A Lack of Amyloid β Plaques Despite Persistent Accumulation of Amyloid β in Axons of Long-Term Survivors of Traumatic Brain Injury. Brain Pathology, 19: 214–223. doi: 10.1111/j.1750-3639.2008.00176.x
- Issue published online: 5 MAR 2009
- Article first published online: 19 MAY 2008
- Received 18 June 2007; accepted 17 March 2008.
- amyloid-precursor protein;
- diffuse axonal injury;
- dystrophic neurites;
- traumatic brain injury
Traumatic brain injury (TBI) is a risk factor for developing Alzheimer's disease (AD). Additionally, TBI induces AD-like amyloid β (Aβ) plaque pathology within days of injury potentially resulting from massive accumulation of amyloid precursor protein (APP) in damaged axons. Here, progression of Aβ accumulation was examined using brain tissue from 23 cases with post-TBI survival of up to 3 years. Even years after injury, widespread axonal pathology was consistently observed and was accompanied by intra-axonal co-accumulations of APP with its cleavage enzymes, beta-site APP cleaving enzyme and presenilin-1 and their product, Aβ. However, in marked contrast to the plaque pathology noted in short-term cases post TBI, virtually no Aβ plaques were found in long-term survivors. A potential mechanism for Aβ plaque regression was suggested by the post-injury accumulation of an Aβ degrading enzyme, neprilysin. These findings fail to support the premise that progressive plaque pathology after TBI ultimately results in AD.