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@ARTICLE{Ciampa:163666,
      author       = {Ciampa, Claire J and Parent, Jourdan H and Harrison,
                      Theresa M and Fain, Rebekah M and Betts, Matthew J and
                      Maaß, Anne and Winer, Joseph R and Baker, Suzanne L and
                      Janabi, Mustafa and Furman, Daniella J and D'Esposito, Mark
                      and Jagust, William J and Berry, Anne S},
      title        = {{A}ssociations among locus coeruleus catecholamines, tau
                      pathology, and memory in aging.},
      journal      = {Neuropsychopharmacology},
      volume       = {47},
      number       = {5},
      issn         = {0893-133X},
      address      = {Basingstoke},
      publisher    = {Nature Publishing Group},
      reportid     = {DZNE-2022-00412},
      pages        = {1106-1113},
      year         = {2022},
      abstract     = {The locus coeruleus (LC) is the brain's major source of the
                      neuromodulator norepinephrine, and is also profoundly
                      vulnerable to the development of Alzheimer's disease
                      (AD)-related tau pathology. Norepinephrine plays a role in
                      neuroprotective functions that may reduce AD progression,
                      and also underlies optimal memory performance. Successful
                      maintenance of LC neurochemical function represents a
                      candidate mechanism of protection against the propagation of
                      AD-related pathology and may facilitate the preservation of
                      memory performance despite pathology. Using
                      [18F]Fluoro-m-tyrosine ([18F]FMT) PET imaging to measure
                      catecholamine synthesis capacity in LC regions of interest,
                      we examined relationships among LC neurochemical function,
                      AD-related pathology, and memory performance in cognitively
                      normal older adults (n = 49). Participants underwent
                      [11C]Pittsburgh compound B and [18F]Flortaucipir PET to
                      quantify β-amyloid (n = 49) and tau burden (n = 42)
                      respectively. In individuals with substantial β-amyloid,
                      higher LC [18F]FMT net tracer influx (Kivis) was associated
                      with lower temporal tau. Longitudinal tau-PET analyses in a
                      subset of our sample (n = 30) support these findings to
                      reveal reduced temporal tau accumulation in the context of
                      higher LC [18F]FMT Kivis. Higher LC catecholamine synthesis
                      capacity was positively correlated with self-reported
                      cognitive engagement and physical activity across the
                      lifespan, established predictors of successful aging
                      measured with the Lifetime Experiences Questionnaire. LC
                      catecholamine synthesis capacity moderated tau's negative
                      effect on memory, such that higher LC catecholamine
                      synthesis capacity was associated with better-than-expected
                      memory performance given an individual's tau burden. These
                      PET findings provide insight into the neurochemical
                      mechanisms of AD vulnerability and cognitive resilience in
                      the living human brain.},
      keywords     = {Aged / Aging: pathology / Alzheimer Disease: diagnostic
                      imaging / Alzheimer Disease: pathology / Amyloid
                      beta-Peptides: metabolism / Catecholamines / Humans / Locus
                      Coeruleus: diagnostic imaging / Locus Coeruleus: metabolism
                      / Norepinephrine / Positron-Emission Tomography: methods /
                      tau Proteins: metabolism / Amyloid beta-Peptides (NLM
                      Chemicals) / Catecholamines (NLM Chemicals) / tau Proteins
                      (NLM Chemicals) / Norepinephrine (NLM Chemicals)},
      cin          = {AG Düzel / AG Maaß},
      ddc          = {610},
      cid          = {I:(DE-2719)5000006 / I:(DE-2719)1311001},
      pnm          = {353 - Clinical and Health Care Research (POF4-353)},
      pid          = {G:(DE-HGF)POF4-353},
      typ          = {PUB:(DE-HGF)16},
      pubmed       = {pmid:35034099},
      pmc          = {pmc:PMC8938463},
      doi          = {10.1038/s41386-022-01269-6},
      url          = {https://pub.dzne.de/record/163666},
}