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@ARTICLE{Richter:841974,
      author       = {Richter, Nils and Beckers, Nora and Onur, Özgür and
                      Dietlein, Markus and Tittgemeyer, Marc and Kracht, Lutz and
                      Neumaier, Bernd and Fink, Gereon Rudolf and Kukolja, Juraj},
      title        = {{E}ffect of cholinergic treatment depends on cholinergic
                      integrity in early {A}lzheimer’s disease},
      journal      = {Brain},
      volume       = {141},
      number       = {3},
      issn         = {1460-2156},
      address      = {Oxford},
      publisher    = {Oxford Univ. Press},
      reportid     = {FZJ-2018-00261},
      pages        = {903–915},
      year         = {2018},
      abstract     = {In early Alzheimer’s disease, which initially presents
                      with progressive loss of short-term memory,
                      neurodegeneration especially affects cholinergic neurons of
                      the basal forebrain. Pharmacotherapy of Alzheimer’s
                      disease therefore often targets the cholinergic system. In
                      contrast, cholinergic pharmacotherapy of mild cognitive
                      impairment is debated since its efficacy to date remains
                      controversial. We here investigated the relationship between
                      cholinergic treatment effects and the integrity of the
                      cholinergic system in mild cognitive impairment due to
                      Alzheimer’s disease. Fourteen patients with high
                      likelihood of mild cognitive impairment due to Alzheimer’s
                      disease and 16 age-matched cognitively normal adults
                      performed an episodic memory task during functional magnetic
                      resonance imaging under three conditions: (i) without
                      pharmacotherapy; (ii) with placebo; and (iii) with a single
                      dose of rivastigmine (3 mg). Cortical acetylcholinesterase
                      activity was measured using PET with the tracer
                      11C-N-methyl-4-piperidyl acetate (MP4A). Cortical
                      acetylcholinesterase activity was significantly decreased in
                      patients relative to controls, especially in the lateral
                      temporal lobes. Without pharmacotherapy, mild cognitive
                      impairment was associated with less memory-related neural
                      activation in the fusiform gyrus and impaired deactivation
                      in the posterior cingulate cortex, relative to controls.
                      These differences were attenuated under cholinergic
                      stimulation with rivastigmine: patients showed increased
                      neural activation in the right fusiform gyrus but enhanced
                      deactivation of the posterior cingulate cortex under
                      rivastigmine, compared to placebo. Conversely, controls
                      showed reduced activation of the fusiform gyrus and reduced
                      deactivation of the posterior cingulate under rivastigmine,
                      compared to placebo. In both groups, the change in neural
                      activation in response to rivastigmine was negatively
                      associated with local acetylcholinesterase activity. At the
                      behavioural level, an analysis of covariance revealed a
                      significant group × treatment interaction in episodic
                      memory performance when accounting for hippocampal grey
                      matter atrophy and function. Our results indicate that
                      rivastigmine differentially affects memory-related neural
                      activity in patients with mild cognitive impairment and
                      cognitively normal, age-matched adults, depending on
                      acetylcholinesterase activity as a marker for the integrity
                      of the cortical cholinergic system. Furthermore, hippocampal
                      integrity showed an independent association with the
                      response of memory performance to acetylcholinesterase
                      inhibition.},
      cin          = {INM-3 / INM-5},
      ddc          = {610},
      cid          = {I:(DE-Juel1)INM-3-20090406 / I:(DE-Juel1)INM-5-20090406},
      pnm          = {572 - (Dys-)function and Plasticity (POF3-572)},
      pid          = {G:(DE-HGF)POF3-572},
      typ          = {PUB:(DE-HGF)16},
      UT           = {WOS:000426813600032},
      pubmed       = {pmid:29309600},
      doi          = {10.1093/brain/awx356},
      url          = {https://juser.fz-juelich.de/record/841974},
}