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@ARTICLE{Simons:265749,
      author       = {Simons, Mikael and Levin, Johannes and Dichgans, Martin},
      title        = {{T}ipping points in neurodegeneration.},
      journal      = {Neuron},
      volume       = {111},
      number       = {19},
      issn         = {0896-6273},
      address      = {New York, NY},
      publisher    = {Elsevier},
      reportid     = {DZNE-2023-01024},
      pages        = {2954 - 2968},
      year         = {2023},
      abstract     = {In Alzheimer's disease (AD), Aβ deposits form slowly,
                      several decades before further pathological events trigger
                      neurodegeneration and dementia. However, a substantial
                      proportion of affected individuals remains non-demented
                      despite AD pathology, raising questions about the underlying
                      factors that determine the transition to clinical disease.
                      Here, we emphasize the critical function of resilience and
                      resistance factors, which we extend beyond the concept of
                      cognitive reserve to include the glial, immune, and vascular
                      system. We review the evidence and use the metaphor of
                      'tipping points' to illustrate how gradually forming AD
                      neuropathology in the preclinical stage can transition to
                      dementia once adaptive functions of the glial, immune, and
                      vascular system are lost and self-reinforcing pathological
                      cascades are unleashed. Thus, we propose an expanded
                      framework for pathomechanistic research that focuses on
                      tipping points and non-neuronal resilience mechanisms, which
                      may represent previously untapped therapeutic targets in
                      preclinical AD.},
      subtyp        = {Review Article},
      keywords     = {Humans / Alzheimer Disease: pathology / Neuroglia:
                      pathology / Amyloid beta-Peptides / Alzheimer's disease
                      (Other) / glia (Other) / inflammation (Other) /
                      neurodegeneration (Other) / vasculature (Other) / Amyloid
                      beta-Peptides (NLM Chemicals)},
      cin          = {AG Dichgans / AG Simons / AG Levin / Clinical Research
                      (Munich)},
      ddc          = {610},
      cid          = {I:(DE-2719)5000022 / I:(DE-2719)1110008 /
                      I:(DE-2719)1111016 / I:(DE-2719)1111015},
      pnm          = {353 - Clinical and Health Care Research (POF4-353) / 351 -
                      Brain Function (POF4-351)},
      pid          = {G:(DE-HGF)POF4-353 / G:(DE-HGF)POF4-351},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:37385247},
      doi          = {10.1016/j.neuron.2023.05.031},
      url          = {https://pub.dzne.de/record/265749},
}