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@ARTICLE{Bacioglu:138738,
      author       = {Bacioglu, Mehtap and Maia, Luis F and Preische, Oliver and
                      Schelle, Juliane and Apel, Anja and Kaeser, Stephan A and
                      Schweighauser, Manuel and Eninger, Timo and Lambert, Marius
                      and Pilotto, Andrea and Shimshek, Derya R and Neumann, Ulf
                      and Kahle, Philipp J and Staufenbiel, Matthias and Neumann,
                      Manuela and Maetzler, Walter and Kuhle, Jens and Jucker,
                      Mathias},
      title        = {{N}eurofilament {L}ight {C}hain in {B}lood and {CSF} as
                      {M}arker of {D}isease {P}rogression in {M}ouse {M}odels and
                      in {N}eurodegenerative {D}iseases.},
      journal      = {Neuron},
      volume       = {91},
      number       = {1},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-05060},
      pages        = {56-66},
      year         = {2016},
      abstract     = {A majority of current disease-modifying
                      therapeutic approaches for age-related neurodegenerative
                      diseases target their characteristic proteopathic lesions
                      (α-synuclein, Tau, Aβ). To monitor such treatments, fluid
                      biomarkers reflecting the underlying disease process are
                      crucial. We found robust increases of neurofilament light
                      chain (NfL) in CSF and blood in murine models of
                      α-synucleinopathies, tauopathy, and β-amyloidosis. Blood
                      and CSF NfL levels were strongly correlated, and NfL
                      increases coincided with the onset and progression of the
                      corresponding proteopathic lesions in brain. Experimental
                      induction of α-synuclein lesions increased CSF and blood
                      NfL levels, while blocking Aβ lesions attenuated the NfL
                      increase. Consistently, we also found NfL increases in CSF
                      and blood of human α-synucleinopathies, tauopathies, and
                      Alzheimer's disease. Our results suggest that CSF and
                      particularly blood NfL can serve as a reliable and easily
                      accessible biomarker to monitor disease progression and
                      treatment response in mouse models and potentially in human
                      proteopathic neurodegenerative diseases.},
      keywords     = {Animals / Axons: metabolism / Biomarkers: blood /
                      Biomarkers: cerebrospinal fluid / Brain: metabolism / Brain:
                      pathology / Disease Progression / Intermediate Filaments:
                      metabolism / Mice, Inbred C57BL / Mice, Transgenic /
                      Neurodegenerative Diseases: diagnosis / Neurodegenerative
                      Diseases: metabolism / Neurodegenerative Diseases: pathology
                      / Neurofilament Proteins: blood / Neurofilament Proteins:
                      cerebrospinal fluid / alpha-Synuclein: metabolism /
                      Biomarkers (NLM Chemicals) / Neurofilament Proteins (NLM
                      Chemicals) / alpha-Synuclein (NLM Chemicals)},
      cin          = {AG Jucker / AG Kahle / Ext UKT-Trend / AG Neumann / AG
                      Maetzler},
      ddc          = {610},
      cid          = {I:(DE-2719)1210001 / I:(DE-2719)1210000-4 /
                      I:(DE-2719)5000056 / I:(DE-2719)1210003 /
                      I:(DE-2719)5000024},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 345
                      - Population Studies and Genetics (POF3-345) / 344 -
                      Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-345 /
                      G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:27292537},
      doi          = {10.1016/j.neuron.2016.05.018},
      url          = {https://pub.dzne.de/record/138738},
}