text: Traumatic brain injury is defined as a “direct physical impact or trauma to
  the head followed by a dynamic series of injury and repair events”.  Recently, neuroproteomics have been applied to studying the disability that over 5.4 million Americans live with.  In addition to physically injuring the brain tissue, traumatic brain injury induces the release of glutamate that interacts with ionotropic glutamate receptors (iGluRs).  These glutamate receptors acidify the surrounding intracranial fluid, causing further injury on the molecular level to nearby neurons.  The death of the surrounding neurons is induced through normal apoptosis mechanisms, and it is this cycle that is being studied with neuroproteomics.  Three different cysteine protease derivatives are involved in the apoptotic pathway induced by the acidic environment triggered by glutamate.  These cysteine proteases include calpain, caspase, and cathepsin.  These three proteins are examples of detectable signs of traumatic brain injury that are much more specific than temperature, oxygen level, or intracranial pressure.
  Proteomics thus also offers a tracking mechanism by which researchers can monitor the progression of traumatic brain injury, or a chronic disease such as Alzheimer’s or Parkinson’s.  Especially in Parkinson’s, in which neurotransmitters play a large role, recent proteomic research has involved the study of synaptotagmin.  Synaptotagmin is involved in the calcium-induced budding of vesicle containing neurotransmitters from the presynaptic membrane.  By studying the intracellular mechanisms involved in neural apoptosis after traumatic brain injury, researchers can create a map that genetic changes can follow later on.