Effect of paroxetine treatment on established amyloid pathology in the APPswe/PS1ΔE9 mouse model of Alzheimer's disease

Finsen, B. (Other), Mithula Sivasaravanaparan (Other), Maurizio Severino (Other), Louise Ørum Olesen (Other), Metaxas, A. (Other), Elena Bouzinova (Other), Babcock, A. (Other), Jørgen Hasselstrøm (Other), Jan Bert Gramsbergen (Other), Ove Wiborg (Other)

Activity: Talks and presentationsConference presentations


Poster Presentation


A dysfunction of the serotoninergic system may contribute to aggravate amyloid pathology, which is a hallmark of Alzheimer’s disease (AD). Previously, prophylactic treatment with the selective serotonin reuptake inhibitor (SSRI) citalopram was found to reduce Aβ load in the APPswe/PS1ΔE9 Tg mouse model of AD when administered from 3 to 7 months of age [1,2]. In addition, treatment with the SSRI paroxetine, resulted in a reduction in Aβ load when paroxetine was administered prophylactically from 5 to 10 months of age in a triple-Tg mouse model of AD [3]. Acute citalopram administration was found to reduce Aβ levels in CSF in young healthy humans in one study [2], but not in another [4]. We investigated if therapeutic treatment with paroxetine can impede the age-dependent increase in Aβ pathology in the APPswe/PS1ΔE9 Tg mouse model of AD, and additionally if toxin-induced deletion of 5-HT neurons influences Aβ pathology in this model.

Literature: [1] Cirrito et al. 2011. Proc Natl Acad Sci 108:14968-73. [2] Sheline et al. 2014. Sci Trans Med 3008169. [3] Nelson et al. 2007. Exp Neurol 205:166-76. [4] Emilsson et al. 2014. Sci Trans Med 268 268le5.
Period11. Nov 2017
Event titleNeuroscience 2017, Society for Neuroscience, Washington DC, USA.
Event typeConference
LocationWashington , United States
Degree of RecognitionInternational