Loss-averse decisions, in which one avoids losses at the expense of gains, are highly prevalent. However, the underlying mechanisms remain controversial. The prevailing account highlights a valuation bias that overweighs losses relative to gains, but an alternative view stresses a response bias to avoid choices involving potential losses. Here we couple a computational process model with eye-tracking and pupillometry to develop a physiologically grounded framework for the decision process leading to accepting or rejecting gambles with equal odds of winning and losing money. Overall, loss-averse decisions were accompanied by preferential gaze toward losses and increased pupil dilation for accepting gambles. Using our model, we found gaze allocation selectively indexed valuation bias, and pupil dilation selectively indexed response bias. Finally, we demonstrate that our computational model and physiological biomarkers can identify distinct types of loss-averse decision makers who would otherwise be indistinguishable using conventional approaches. Our study provides an integrative framework for the cognitive processes that drive loss-averse decisions and highlights the biological heterogeneity of loss aversion across individuals.

Highlights We present a new imaging study of 200 adults experiencing depression and anxiety. Quantitative measures of image quality indicate comparable quality to the HCP-YA. In addition, a comprehensive set of assessments measured patients’ symptom profiles. Data will be publicly available through the NIMH Data Archive starting fall 2020.

ObjectiveTo determine whether compared with placebo, treatment with escitalopram (ESC) would lower CSF (CSF) amyloid beta 42 (Aβ42) levels.RationaleSerotonin signaling suppresses Aβ42 in animal models of Alzheimer's disease (AD) and young healthy humans. In a prospective study in older adults, we examined dose and treatment duration effects of ESC.MethodsUsing lumbar punctures (LPs) to sample CSF levels before and after a course of ESC treatment, cognitively normal older adults (n = 114) were assigned to either: placebo; 20 mg ESC × 2 weeks; 20 mg ESC × 8 weeks or 30 mg ESC × 8 weeks with CSF sampled pre- and post-treatment and within-subject percent change in Aβ42 was used as the primary outcome in subsequent analyses.ResultsAn overall 9.4% percentage point greater reduction in CSF Aβ42 was found in ESC treated compared with placebo treated groups (p < 0.001; 95% CI [4.9%–14.2%]; d = 0.81). Positive baseline amyloid-beta status (CSF Aβ42 levels <250 pg/mL) was associated with smaller Aβ42 reduction (p = 0.006; 95% CI [−16.7% to 0.5%]; d = −0.52) compared with negative baseline amyloid status (CSF Aβ42 levels >250 pg/mL).ConclusionsShort-term longitudinal doses of ESC decreased CSF Aβ42 in cognitively normal older adults, the target group for AD prevention.Classification of evidenceThis study provides Class II evidence that for cognitively normal older adults, ESC decreases CSF Aβ42.Clinical trial identifierNCT02161458.

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