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@ARTICLE{Mller:156008,
      author       = {Müller, Luisa and Power Guerra, Nicole and Stenzel, Jan
                      and Rühlmann, Claire and Lindner, Tobias and Krause, Bernd
                      J and Vollmar, Brigitte and Teipel, Stefan and Kuhla,
                      Angela},
      title        = {{L}ong-{T}erm {C}aloric {R}estriction {A}ttenuates
                      β-{A}myloid {N}europathology and {I}s {A}ccompanied by
                      {A}utophagy in {APP}swe/{PS}1delta9 {M}ice.},
      journal      = {Nutrients},
      volume       = {13},
      number       = {3},
      issn         = {2072-6643},
      address      = {Basel},
      publisher    = {MDPI},
      reportid     = {DZNE-2021-01140},
      pages        = {985},
      year         = {2021},
      abstract     = {Caloric restriction (CR) slows the aging process, extends
                      lifespan, and exerts neuroprotective effects. It is widely
                      accepted that CR attenuates β-amyloid (Aβ) neuropathology
                      in models of Alzheimer's disease (AD) by so-far unknown
                      mechanisms. One promising process induced by CR is
                      autophagy, which is known to degrade aggregated proteins
                      such as amyloids. In addition, autophagy positively
                      regulates glucose uptake and may improve cerebral
                      hypometabolism-a hallmark of AD-and, consequently, neural
                      activity. To evaluate this hypothesis, APPswe/PS1delta9 (tg)
                      mice and their littermates (wild-type, wt) underwent CR for
                      either 16 or 68 weeks. Whereas short-term CR for 16 weeks
                      revealed no noteworthy changes of AD phenotype in tg mice,
                      long-term CR for 68 weeks showed beneficial effects. Thus,
                      cerebral glucose metabolism and neuronal integrity were
                      markedly increased upon 68 weeks CR in tg mice, indicated by
                      an elevated hippocampal fluorodeoxyglucose [18F] ([18F]FDG)
                      uptake and increased N-acetylaspartate-to-creatine ratio
                      using positron emission tomography/computer tomography
                      (PET/CT) imaging and magnet resonance spectroscopy (MRS).
                      Improved neuronal activity and integrity resulted in a
                      better cognitive performance within the Morris Water Maze.
                      Moreover, CR for 68 weeks caused a significant increase of
                      LC3BII and p62 protein expression, showing enhanced
                      autophagy. Additionally, a significant decrease of Aβ
                      plaques in tg mice in the hippocampus was observed,
                      accompanied by reduced microgliosis as indicated by
                      significantly decreased numbers of iba1-positive cells. In
                      summary, long-term CR revealed an overall neuroprotective
                      effect in tg mice. Further, this study shows, for the first
                      time, that CR-induced autophagy in tg mice accompanies the
                      observed attenuation of Aβ pathology.},
      keywords     = {Alzheimer Disease: diet therapy / Alzheimer Disease:
                      pathology / Amyloid beta-Peptides: metabolism / Animal
                      Nutritional Physiological Phenomena / Animals / Aspartic
                      Acid: analogs $\&$ derivatives / Aspartic Acid: metabolism /
                      Autophagy: physiology / Calcium-Binding Proteins: metabolism
                      / Caloric Restriction: methods / Cerebral Cortex: metabolism
                      / Creatine: metabolism / Disease Models, Animal /
                      Fluorodeoxyglucose F18 / Glucose: metabolism / Hippocampus:
                      diagnostic imaging / Hippocampus: metabolism / Magnetic
                      Resonance Spectroscopy / Maze Learning / Mice / Mice, Inbred
                      C3H / Mice, Inbred C57BL / Mice, Transgenic / Microfilament
                      Proteins: metabolism / Neurons: physiology / Plaque,
                      Amyloid: diet therapy / Plaque, Amyloid: pathology /
                      Positron Emission Tomography Computed Tomography /
                      Radiopharmaceuticals / APPswe/PS1delta9 (Other) /
                      [18F]FDG-PET/CT (Other) / amyloid β (Other) / autophagy
                      (Other) / caloric restriction (Other) / iba1 (Other) / Aif1
                      protein, mouse (NLM Chemicals) / Amyloid beta-Peptides (NLM
                      Chemicals) / Calcium-Binding Proteins (NLM Chemicals) /
                      Microfilament Proteins (NLM Chemicals) /
                      Radiopharmaceuticals (NLM Chemicals) / Fluorodeoxyglucose
                      F18 (NLM Chemicals) / Aspartic Acid (NLM Chemicals) /
                      N-acetylaspartate (NLM Chemicals) / Glucose (NLM Chemicals)
                      / Creatine (NLM Chemicals)},
      cin          = {AG Teipel},
      ddc          = {610},
      cid          = {I:(DE-2719)1510100},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:33803798},
      pmc          = {pmc:PMC8003277},
      doi          = {10.3390/nu13030985},
      url          = {https://pub.dzne.de/record/156008},
}