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@ARTICLE{OldeHeuvel:272981,
      author       = {Olde Heuvel, Florian and Li, Zhenghui and Riedel, Daniel
                      and Halbgebauer, Steffen and Oeckl, Patrick and Mayer,
                      Benjamin and Gotzman, Nina and Shultz, Sandy and Semple,
                      Bridgette and Tumani, Hayrettin and Ludolph, Albert C and
                      Böckers, Tobias and Morganti-Kossmann, Cristina and Otto,
                      Markus and Roselli, Francesco},
      title        = {{D}ynamics of synaptic damage in severe traumatic brain
                      injury revealed by cerebrospinal fluid {SNAP}-25 and
                      {VILIP}-1.},
      journal      = {Journal of neurology, neurosurgery, and psychiatry},
      volume       = {95},
      number       = {12},
      issn         = {0022-3050},
      address      = {London},
      publisher    = {BMJ Publishing Group},
      reportid     = {DZNE-2024-01360},
      pages        = {1158 - 1167},
      year         = {2024},
      abstract     = {Biomarkers of neuronal, glial cells and inflammation in
                      traumatic brain injury (TBI) are available but they do not
                      specifically reflect the damage to synapses, which represent
                      the bulk volume of the brain. Experimental models have
                      demonstrated extensive involvement of synapses in acute TBI,
                      but biomarkers of synaptic damage in human patients have not
                      been explored.Single-molecule array assays were used to
                      measure synaptosomal-associated protein-25 (SNAP-25) and
                      visinin-like protein 1 (VILIP-1) (along with neurofilament
                      light chain (NFL), ubiquitin carboxy-terminal hydrolase L1
                      (UCH-L1), glial fibrillar acidic protein (GFAP),
                      interleukin-6 (IL-6) and interleukin-8 (IL-8)) in
                      ventricular cerebrospinal fluid (CSF) samples longitudinally
                      acquired during the intensive care unit (ICU) stay of 42
                      patients with severe TBI or 22 uninjured controls.CSF levels
                      of SNAP-25 and VILIP-1 are strongly elevated early after
                      severe TBI and decline in the first few days. SNAP-25 and
                      VILIP-1 correlate with inflammatory markers at two distinct
                      timepoints (around D1 and then again at D5) in follow-up.
                      SNAP-25 and VILIP-1 on the day-of-injury have better
                      sensitivity and specificity for unfavourable outcome at 6
                      months than NFL, UCH-L1 or GFAP. Later elevation of SNAP-25
                      was associated with poorer outcome.Synaptic damage markers
                      are acutely elevated in severe TBI and predict long-term
                      outcomes, as well as, or better than, markers of neuroaxonal
                      injury. Synaptic damage correlates with initial injury and
                      with a later phase of secondary inflammatory injury.},
      keywords     = {Humans / Brain Injuries, Traumatic: cerebrospinal fluid /
                      Synaptosomal-Associated Protein 25: cerebrospinal fluid /
                      Male / Adult / Female / Biomarkers: cerebrospinal fluid /
                      Middle Aged / Neurocalcin: cerebrospinal fluid / Synapses:
                      pathology / Neurofilament Proteins: cerebrospinal fluid /
                      Ubiquitin Thiolesterase: cerebrospinal fluid / Glial
                      Fibrillary Acidic Protein: cerebrospinal fluid /
                      Interleukin-6: cerebrospinal fluid / Young Adult / Aged /
                      traumatic brain injury (Other) / Synaptosomal-Associated
                      Protein 25 (NLM Chemicals) / Biomarkers (NLM Chemicals) /
                      Neurocalcin (NLM Chemicals) / neurofilament protein L (NLM
                      Chemicals) / VSNL1 protein, human (NLM Chemicals) /
                      Neurofilament Proteins (NLM Chemicals) / SNAP25 protein,
                      human (NLM Chemicals) / Ubiquitin Thiolesterase (NLM
                      Chemicals) / Glial Fibrillary Acidic Protein (NLM Chemicals)
                      / Interleukin-6 (NLM Chemicals) / UCHL1 protein, human (NLM
                      Chemicals) / GFAP protein, human (NLM Chemicals)},
      cin          = {AG Roselli / Clinical Study Center (Ulm)},
      ddc          = {610},
      cid          = {I:(DE-2719)1910001 / I:(DE-2719)5000077},
      pnm          = {352 - Disease Mechanisms (POF4-352) / 353 - Clinical and
                      Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-352 / G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pmc          = {pmc:PMC11671962},
      pubmed       = {pmid:38825349},
      doi          = {10.1136/jnnp-2024-333413},
      url          = {https://pub.dzne.de/record/272981},
}