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@ARTICLE{deSouzaSilva:137038,
      author       = {de Souza Silva, Maria A and Lenz, Bernd and Rotter, Andrea
                      and Biermann, Teresa and Peters, Oliver and Ramirez, Alfredo
                      and Jessen, Frank and Maier, Wolfgang and Hüll, Michael and
                      Schröder, Johannes and Frölich, Lutz and Teipel, Stefan
                      and Gruber, Oliver and Kornhuber, Johannes and Huston,
                      Joseph P and Müller, Christian P and Schäble, Sandra},
      title        = {{N}eurokinin3 receptor as a target to predict and improve
                      learning and memory in the aged organism.},
      journal      = {Proceedings of the National Academy of Sciences of the
                      United States of America},
      volume       = {110},
      number       = {37},
      issn         = {0027-8424},
      address      = {Washington, DC},
      publisher    = {National Acad. of Sciences},
      reportid     = {DZNE-2020-03360},
      pages        = {15097-15102},
      year         = {2013},
      abstract     = {Impaired learning and memory performance is often found in
                      aging as an early sign of dementia. It is associated with
                      neuronal loss and reduced functioning of cholinergic
                      networks. Here we present evidence that the neurokinin3
                      receptors (NK3-R) and their influence on acetylcholine (ACh)
                      release may represent a crucial mechanism that underlies
                      age-related deficits in learning and memory. Repeated
                      pharmacological stimulation of NK3-R in aged rats was found
                      to improve learning in the water maze and in object-place
                      recognition. This treatment also enhanced in vivo
                      acetylcholinergic activity in the frontal cortex,
                      hippocampus, and amygdala but reduced NK3-R mRNA expression
                      in the hippocampus. Furthermore, NK3-R agonism incurred a
                      significantly higher increase in ACh levels in aged animals
                      that showed superior learning than in those that were most
                      deficient in learning. Our findings suggest that the induced
                      activation of ACh, rather than basal ACh activity, is
                      associated with superior learning in the aged. To test
                      whether natural variation in NK3-R function also determines
                      learning and memory performance in aged humans, we
                      investigated 209 elderly patients with cognitive
                      impairments. We found that of the 15 analyzed single
                      single-nucleotide ploymorphism (SNPs) of the NK3-R-coding
                      gene, TACR3, the rs2765 SNP predicted the degree of
                      impairment of learning and memory in these patients. This
                      relationship could be partially explained by a reduced right
                      hippocampus volume in a subsample of 111 tested dementia
                      patients. These data indicate the NK3-R as an important
                      target to predict and improve learning and memory
                      performance in the aged organism.},
      keywords     = {Acetylcholine: physiology / Aged / Aged, 80 and over /
                      Aging: genetics / Aging: physiology / Aging: psychology /
                      Animals / Cognition Disorders: genetics / Cognition
                      Disorders: physiopathology / Cognition Disorders: psychology
                      / Cognitive Dysfunction: genetics / Cognitive Dysfunction:
                      physiopathology / Cognitive Dysfunction: psychology /
                      Dementia: genetics / Dementia: physiopathology / Dementia:
                      psychology / Female / Genetic Association Studies / Humans /
                      Learning: drug effects / Learning: physiology / Male / Maze
                      Learning: drug effects / Maze Learning: physiology / Memory:
                      drug effects / Memory: physiology / Middle Aged / Models,
                      Animal / Models, Neurological / Polymorphism, Single
                      Nucleotide / RNA, Messenger: genetics / RNA, Messenger:
                      metabolism / Rats / Rats, Wistar / Receptors, Neurokinin-3:
                      agonists / Receptors, Neurokinin-3: genetics / Receptors,
                      Neurokinin-3: physiology / RNA, Messenger (NLM Chemicals) /
                      Receptors, Neurokinin-3 (NLM Chemicals) / Acetylcholine (NLM
                      Chemicals)},
      cin          = {AG Jessen / U Clinical Researchers - Bonn / Clinical
                      Dementia Research Rostock /Greifswald ; AG Teipel},
      ddc          = {500},
      cid          = {I:(DE-2719)1011102 / I:(DE-2719)7000001 /
                      I:(DE-2719)1510100},
      pnm          = {344 - Clinical and Health Care Research (POF3-344)},
      pid          = {G:(DE-HGF)POF3-344},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:23983264},
      pmc          = {pmc:PMC3773732},
      doi          = {10.1073/pnas.1306884110},
      url          = {https://pub.dzne.de/record/137038},
}