Collated data in cognitively normal individuals suggest that increased brain Aβ is linked to a higher rate of cognitive decline; the increase in amyloid load may occur years before the onset of cognitive symptoms. Many studies have shown a link between serotonin and Aβ. Activation of serotonin receptors has been shown to impair Aβ production in vitro, whereas modulation of serotonin levels in vivo with SSRIs reduces Aβ levels in brain interstitial fluid (BIF) of young APP/PS1 mice. Chronic treatment with SSRIs over a 4-month period has been shown to reduce Aβ plaque burden by 50% in mice. In humans, using PET scans, patients treated with SSRIs during a previous depressive episode up to five years earlier were shown to have lower Aβ deposits than patients not exposed to SSRIs. Therefore, a recent study sought to determine the effects of the SSRI, citalopram, on Aβ levels in mouse models of Alzheimer’s disease (AD) and in healthy young humans. In an aged transgenic mouse model of AD, citalopram was found to lower brain Aβ levels in a dose-dependent manner. In addition, citalopram stopped the growth of pre-existing brain amyloid plaques and reduced the appearance of new plaques by 78%. In healthy human volunteers, the effects of citalopram on Aβ production and cerebrospinal fluid (CSF) Aβ concentrations were measured prospectively. CSF Aβ production was slowed by 37% in the citalopram group compared with placebo, and a 38% decrease in total CSF Aβ concentrations was observed. The ability of this SSRI to safely decrease Aβ concentrations is surely important in preventing AD

About the Author



2004- MS, psychology- Walden University, Minneapolis, MN