2004
DOI: 10.1055/s-2003-43051
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Fluoxetine in Alzheimer's Disease with Severe Obsessive Compulsive Symptoms and a Low Density of Serotonin Transporter Sites

Abstract: The treatment of behavioral disturbances is particularly challenging in patients suffering from dementia. In an 80-year-old female patient with probable AD and severe obsessive and compulsive symptoms, we demonstrated a significant reduction in the density of serotonin transporter sites using 1231-beta-CIT SPECT. Treatment with fluoxetine for 6 months resulted in significant symptom relief and an increasing density of serotonin transporter sites when compared to the beginning of treatment. Therefore, this repo… Show more

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Cited by 20 publications
(6 citation statements)
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“…Only a single case study was reported with SERT imaging using [ 123 I] -CIT in a female patient with probable AD and severe obsessive and compulsive symptoms [609]. A decrease in SERT availability was found.…”
Section: Serotonin Transporter Imaging In Neurological Diseasesmentioning
confidence: 99%
“…Only a single case study was reported with SERT imaging using [ 123 I] -CIT in a female patient with probable AD and severe obsessive and compulsive symptoms [609]. A decrease in SERT availability was found.…”
Section: Serotonin Transporter Imaging In Neurological Diseasesmentioning
confidence: 99%
“…Acute stress activates the hypothalamic-pituitary-adrenal (HPA) axis, as well as monoaminergic neurotransmission in the brain, and affects the expression of numerous genes, including brain-derived neurotrophic factor ( BDNF ) (Pacák and Palkovits, 2001). Dysfunctions of the HPA axis (Phillips et al, 2006; Ströhle and Holsboer, 2003), monoaminergic neurotransmission (Delgado and Moreno, 2000; Graef, 2003; Southwick et al, 1999), GABAergic neurotransmission (Cameron and Nesse, 1988), and abnormal expression of BDNF transcripts (Duman and Monteggia, 2006) have been observed in some stress-related psychiatric disorders. However, it remains to be seen which of these changes are critical causal events mediating the pathophysiological mechanisms underlying stress-related psychiatric disorders.…”
Section: Introductionmentioning
confidence: 99%
“…An increase in cell apoptosis in the hippocampus attenuates negative feedback inhibition of the hippocampus on the HPA axis, in turn, stimulating the release of more CORT [ 39 ]. On the other hand, a state of depression can make the HPA axis hyperactive, and alleviating clinical symptoms can have a normalizing effect on the HPA axis [ 40 , 41 ]. Thus, restoration of HPA axis activity may be a feasible treatment strategy for depression.…”
Section: Discussionmentioning
confidence: 99%