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@ARTICLE{AmbradGiovannetti:140525,
      author       = {Ambrad Giovannetti, Eleonora and Fuhrmann, Martin},
      title        = {{U}nsupervised excitation: {GABA}ergic dysfunctions in
                      {A}lzheimer's disease.},
      journal      = {Brain research},
      volume       = {1707},
      issn         = {0006-8993},
      address      = {Amsterdam},
      publisher    = {Elsevier},
      reportid     = {DZNE-2020-06847},
      pages        = {216-226},
      year         = {2019},
      abstract     = {Alzheimer's disease (AD) is characterized by the classical
                      hallmarks of Aβ-deposition and tau-pathology that are
                      thought to ultimately lead to synapse and neuron loss.
                      Although long known, neuroinflammation has recently
                      attracted a substantial amount of attention by researchers
                      due to genome wide association studies (GWAS) that
                      identified microglia associated genes to be correlated with
                      sporadic AD. Besides that, cholinergic degeneration and
                      gamma-aminobutyric acid (GABA) abnormalities have been
                      identified in the brains of AD patients already decades ago,
                      but have not received much attention over the last ten
                      years. Recently, the neuronal network dysfunction hypothesis
                      has revived interest in how impairments of neuronal
                      communication at the network level lead to epileptiform
                      activity and disrupted oscillations observed in the brains
                      of AD patients and mouse models. Thereby, deficits in
                      neuronal networks involved in learning and memory might
                      ultimately cause memory impairments. In this context, an
                      imbalance between excitation and inhibition has been
                      hypothesized to contribute to neuronal network dysfunction.
                      Here, disturbances of cholinergic and GABAergic transmission
                      might play a crucial role. In this review, we will focus on
                      GABAergic dysfunction in AD and mouse models of AD and how
                      those might relate to neuronal network aberration and memory
                      impairment.},
      subtyp        = {Review Article},
      keywords     = {Alzheimer Disease: physiopathology / Amyloid beta-Peptides:
                      metabolism / Animals / Brain: metabolism / Disease Models,
                      Animal / GABAergic Neurons: metabolism / Humans / Memory:
                      physiology / Memory Disorders: pathology / Nerve
                      Degeneration: pathology / Nerve Net: physiopathology /
                      Neurons: metabolism / gamma-Aminobutyric Acid: metabolism /
                      tau Proteins: metabolism},
      cin          = {AG Fuhrmann},
      ddc          = {610},
      cid          = {I:(DE-2719)1011004},
      pnm          = {342 - Disease Mechanisms and Model Systems (POF3-342)},
      pid          = {G:(DE-HGF)POF3-342},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:30503351},
      doi          = {10.1016/j.brainres.2018.11.042},
      url          = {https://pub.dzne.de/record/140525},
}