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@ARTICLE{Busche:138871,
      author       = {Busche, M. A. and Staufenbiel, M. and Willem, M. and Haass,
                      C. and Förstl, H.},
      title        = {[{M}echanisms of {A}lzheimer's disease : {N}euronal
                      hyperactivity and hypoactivity as new therapeutic targets].},
      journal      = {Der Nervenarzt},
      volume       = {87},
      number       = {11},
      issn         = {0028-2804},
      address      = {Heidelberg},
      publisher    = {Springer},
      reportid     = {DZNE-2020-05193},
      pages        = {1163-1174},
      year         = {2016},
      abstract     = {Alzheimer's disease (AD) is characterized by the
                      pathological accumulation of amyloid-beta (Abeta) and tau
                      peptides in the brain. Recent evidence suggests that the
                      soluble peptide amyloid-eta (Aeta) may have an additional
                      role in the pathogenesis of AD. The detailed investigation
                      of the cellular and neurophysiological mechanisms underlying
                      AD has revealed surprising results that may become highly
                      relevant for the early diagnosis and treatment of the
                      disease. By analyzing the function of single neurons and
                      large-scale networks in intact brains in vivo it has been
                      shown that A-beta, tau and A-eta abnormally modulate brain
                      activity and obviously unfold contrasting effects: while
                      A-beta promotes neuronal hyperactivity as well as
                      epileptiform activity, tau and A-eta reduce the activity of
                      neurons. Promising new evidence from animal studies and
                      humans with AD indicates that the treatment of hyperactivity
                      may improve cognitive dysfunctions and even slow the
                      underlying disease process.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer Disease: complications / Alzheimer Disease:
                      physiopathology / Alzheimer Disease: therapy / Brain:
                      physiopathology / Evidence-Based Medicine / Humans /
                      Psychomotor Agitation: complications / Psychomotor
                      Agitation: physiopathology / Psychomotor Agitation: therapy
                      / Treatment Outcome},
      cin          = {Ext LMU / AG Haass},
      ddc          = {610},
      cid          = {I:(DE-2719)5000048 / I:(DE-2719)1110007},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:26781314},
      doi          = {10.1007/s00115-015-0041-5},
      url          = {https://pub.dzne.de/record/138871},
}