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@ARTICLE{Heneka:137851,
      author       = {Heneka, Michael and Carson, Monica J and El Khoury, Joseph
                      and Landreth, Gary E and Brosseron, Frederic and Feinstein,
                      Douglas L and Jacobs, Andreas H and Wyss-Coray, Tony and
                      Vitorica, Javier and Ransohoff, Richard M and Herrup, Karl
                      and Frautschy, Sally A and Finsen, Bente and Brown, Guy C
                      and Verkhratsky, Alexei and Yamanaka, Koji and Koistinaho,
                      Jari and Latz, Eicke and Halle, Annett and Petzold, Gabor C
                      and Town, Terrence and Morgan, Dave and Shinohara, Mari L
                      and Perry, V Hugh and Holmes, Clive and Bazan, Nicolas G and
                      Brooks, David J and Hunot, Stéphane and Joseph, Bertrand
                      and Deigendesch, Nikolaus and Garaschuk, Olga and Boddeke,
                      Erik and Dinarello, Charles A and Breitner, John C and Cole,
                      Greg M and Golenbock, Douglas T and Kummer, Markus P},
      title        = {{N}euroinflammation in {A}lzheimer's disease.},
      journal      = {The lancet / Neurology},
      volume       = {14},
      number       = {4},
      issn         = {1474-4422},
      address      = {London},
      publisher    = {Lancet Publ. Group},
      reportid     = {DZNE-2020-04173},
      pages        = {388-405},
      year         = {2015},
      abstract     = {Increasing evidence suggests that Alzheimer's disease
                      pathogenesis is not restricted to the neuronal compartment,
                      but includes strong interactions with immunological
                      mechanisms in the brain. Misfolded and aggregated proteins
                      bind to pattern recognition receptors on microglia and
                      astroglia, and trigger an innate immune response
                      characterised by release of inflammatory mediators, which
                      contribute to disease progression and severity. Genome-wide
                      analysis suggests that several genes that increase the risk
                      for sporadic Alzheimer's disease encode factors that
                      regulate glial clearance of misfolded proteins and the
                      inflammatory reaction. External factors, including systemic
                      inflammation and obesity, are likely to interfere with
                      immunological processes of the brain and further promote
                      disease progression. Modulation of risk factors and
                      targeting of these immune mechanisms could lead to future
                      therapeutic or preventive strategies for Alzheimer's
                      disease.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer Disease: genetics / Alzheimer Disease: immunology
                      / Alzheimer Disease: metabolism / Alzheimer Disease:
                      pathology / Alzheimer Disease: prevention $\&$ control /
                      Animals / Anti-Inflammatory Agents, Non-Steroidal:
                      therapeutic use / Astrocytes: immunology / Astrocytes:
                      pathology / Biomarkers: blood / Biomarkers: cerebrospinal
                      fluid / Brain Injuries: complications / Brain Injuries:
                      metabolism / Clinical Trials as Topic / Disease Models,
                      Animal / Disease Progression / Humans / Immunity, Innate /
                      Immunization / Inflammation: diagnosis / Inflammation:
                      immunology / Inflammation: metabolism / Inflammation
                      Mediators: immunology / Inflammation Mediators: metabolism /
                      Locus Coeruleus: pathology / Microglia: immunology /
                      Microglia: pathology / Nootropic Agents: administration $\&$
                      dosage / Obesity: complications / Obesity: metabolism /
                      Phagocytosis / Protein Folding / Risk Factors / Severity of
                      Illness Index / Anti-Inflammatory Agents, Non-Steroidal (NLM
                      Chemicals) / Biomarkers (NLM Chemicals) / Inflammation
                      Mediators (NLM Chemicals) / Nootropic Agents (NLM
                      Chemicals)},
      cin          = {AG Heneka ; AG Heneka / AG Latz ; AG Latz / AG Petzold ; AG
                      Petzold},
      ddc          = {610},
      cid          = {I:(DE-2719)1011303 / I:(DE-2719)1013024 /
                      I:(DE-2719)1013020},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342) / 344
                      - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-342 / G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:25792098},
      pmc          = {pmc:PMC5909703},
      doi          = {10.1016/S1474-4422(15)70016-5},
      url          = {https://pub.dzne.de/record/137851},
}