@article{GulbinsPalmadaReicheletal.2013,
  author    = {Gulbins, Erich and Palmada, Monica and Reichel, Martin and Lueth, Anja and Boehmer, Christoph and Amato, Davide and Mueller, Christian P. and Tischbirek, Carsten H. and Groemer, Teja W. and Tabatabai, Ghazaleh and Becker, Katrin Anne and Tripal, Philipp and Staedtler, Sven and Ackermann, Teresa F. and van Brederode, Johannes and Alzheimer, Christian and Weller, Michael and Lang, Undine E. and Kleuser, Burkhard and Grassme, Heike and Kornhuber, Johannes},
  title     = {Acid sphingomyelinase-ceramide system mediates effects of antidepressant drugs},
  series = {Nature medicine},
  volume    = {19},
  journal   = {Nature medicine},
  number    = {7},
  publisher = {Nature Publ. Group},
  address   = {New York},
  issn      = {1078-8956},
  doi       = {10.1038/nm.3214},
  pages     = {934 -- +},
  year      = {2013},
  abstract  = {Major depression is a highly prevalent severe mood disorder that is treated with antidepressants. The molecular targets of antidepressants require definition. We investigated the role of the acid sphingomyelinase (Asm)-ceramide system as a target for antidepressants. Therapeutic concentrations of the antidepressants amitriptyline and fluoxetine reduced Asm activity and ceramide concentrations in the hippocampus, increased neuronal proliferation, maturation and survival and improved behavior in mouse models of stress-induced depression. Genetic Asm deficiency abrogated these effects. Mice overexpressing Asm, heterozygous for acid ceramidase, treated with blockers of ceramide metabolism or directly injected with C16 ceramide in the hippocampus had higher ceramide concentrations and lower rates of neuronal proliferation, maturation and survival compared with controls and showed depression-like behavior even in the absence of stress. The decrease of ceramide abundance achieved by antidepressant-mediated inhibition of Asm normalized these effects. Lowering ceramide abundance may thus be a central goal for the future development of antidepressants.},
  language  = {en}
}
@article{MajicGutzmannHeinzetal.2013,
  author    = {Majic, Tomislav and Gutzmann, Hans and Heinz, Andreas and Lang, Undine E. and Rapp, Michael A.},
  title     = {Animal-assisted therapy and agitation and depression in nursing home residents with dementia - a matched case-control trial},
  series = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  volume    = {21},
  journal   = {The American journal of geriatric psychiatry : official journal of the American Association for Geriatric Psychiatry},
  number    = {11},
  publisher = {Lippincott Williams \& Wilkins},
  address   = {Philadelphia},
  issn      = {1064-7481},
  doi       = {10.1016/j.jagp.2013.03.004},
  pages     = {1052 -- 1059},
  year      = {2013},
  abstract  = {Objectives: To investigate the efficacy of animal-assisted therapy (AAT) on symptoms of agitation/aggression and depression in nursing home residents with dementia in a randomized controlled trial. Previous studies have indicated that AAT has beneficial effects on neuropsychiatric symptoms in various psychiatric disorders but few studies have investigated the efficacy of AAT in patients suffering from dementia. Methods: Of 65 nursing home residents with dementia (mean [standard deviation] age: 81.8 [9.2] years; mean Mini-Mental State Examination score: 7.1 [0.7]), 27 matched pairs (N = 54) were randomly assigned to either treatment as usual or treatment as usual combined with AAT, administered over 10 weekly sessions. Blinded raters assessed cognitive impairment with the Mini-Mental State Examination, presence of agitation/aggression with the Cohen-Mansfield Agitation Inventory, and depression with the Dementia Mood Assessment Scale at baseline and during a period of 4 weeks after AAT intervention. Results: In the control group, symptoms of agitation/aggression and depression significantly increased over 10 weeks; in the intervention group, patients receiving combined treatment displayed constant frequency and severity of symptoms of agitation/aggression (F-1,F-48 = 6.43; p <0.05) and depression (F-1,F-48 = 26.54; p <0.001). Symptom amelioration did not occur in either group. Conclusions: AAT is a promising option for the treatment of agitation/aggression and depression in patients with dementia. Our results suggest that AAT may delay progression of neuropsychiatric symptoms in demented nursing home residents. Further research is needed to determine its long-time effects.},
  language  = {en}
}