Skip to main content
. Author manuscript; available in PMC: 2015 Jul 24.
Published in final edited form as: Nat Rev Neurol. 2013 Feb 12;9(4):201–210. doi: 10.1038/nrneurol.2013.9

Figure 1.

Figure 1

Possible biomarkers of traumatic brain injury. These molecules include NSE, SBPs and UCH-L1, which are all enriched in the neuronal cytoplasm. NFL is a biomarker of injury to large-calibre myelinated axons. Total tau is a biomarker of injury to thin nonmyelinated axons. APP and amyloid-β are produced in axon terminals and might be involved in synaptic activity and plasticity. Overproduction of amyloid-β in response to trauma could result in formation of diffuse amyloid plaques. Injury to astroglial cells may lead to release of S100-B and GFAP into the extracellular matrix, which might increase S100-B levels in both cerebrospinal fluid and blood. Astrogliosis and post-injury neuroinflammation can result in increased production of interleukins and cytokines. Integrity of the blood–brain barrier is indicated by the cerebrospinal fluid:serum albumin ratio. Abbreviations: APP, amyloid precursor protein; GFAP, glial fibrillary acidic protein; MBP, myelin basic protein; NFL, neurofilament light polypeptide; NSE, γ-enolase; SBPs, spectrin breakdown products; UCH-L1, ubiquitin carboxyl-terminal hydrolase isoenzyme L1.