Stress could increase delay discounting in subjects with bulimia nervosa and alcohol use disorder (AUD), meaning that the short-term benefits of coping through eating or drinking outweigh the long-term negative consequences. Therefore, this study explores differences in delay discounting between patients and healthy controls, the impact of stress on food and alcohol delay discounting and associated changes in brain activity.

A total of 102 female participants (AUD, 27; bulimia nervosa, 25; healthy controls, 50) underwent repeated functional magnetic resonance imaging scanning. Initially, all participants performed a monetary delay discounting task (DDT), followed by a food or alcohol DDT before and after stress induction. Specifically, those with bulimia nervosa completed a food DDT, those with AUD completed an alcohol DDT and healthy controls were randomly allocated to one or either DDT.

Participants with AUD, but not healthy controls, displayed a higher discounting of alcohol after stress. Healthy controls, but not those with bulimia nervosa, had nominally higher discounting rates of food following stress, although not significant following multiple testing correction. Participants with AUD displayed a lower activity of the right supplementary motor area while discounting alcohol after stress. Healthy controls showed a lower activity of the frontal cortex and a higher activity of the motor cortex while discounting food after stress, while those with bulimia nervosa displayed a higher activity of the occipital cortex.

The results suggest that, in subjects with AUD, stress induces neurobiological changes that cause them to prefer more immediately available alcohol. However, the results observed in participants with bulimia nervosa suggest a more complex relation between stress and food.

Late-life depression (LLD) is characterized by medial temporal lobe (MTL) abnormalities. Although gray matter (GM) and white matter (WM) differences in LLD have been reported, few studies have investigated them concurrently. Moreover, the impact of aetiological factors, such as neurodegenerative and cerebrovascular burden, on tissue differences remains elusive.

This prospective cross-sectional study involved 72 participants, including 33 patients with LLD (mean age 72.2 years, 23 female) and 39 healthy controls (HCs) (mean age 70.6 years, 24 female), who underwent clinical and positron emission tomography (PET)-magnetic resonance imaging (MRI) assessments. High-resolution 3D T1-weighted and T2-weighted FLAIR images were used to assess MTL GM volumes and white matter hyperintensities (WMHs), a proxy for cerebrovascular burden. Diffusion kurtosis imaging metrics derived from multishell diffusion MRI data were analyzed to assess WM microstructure in the following MTL bundles reconstructed using constrained spherical deconvolution tractography: uncinate fasciculus, fornix, and cingulum. Standardized uptake value ratio of 18F-MK-6240 in the MTL was used to assess Alzheimer’s disease (AD) type tau accumulation as a proxy for neurodegenerative burden.

Compared to HCs, patients with LLD showed significantly lower bilateral MTL volumes and WM microstructural differences primarily in the uncinate fasciculi bilaterally and right fornix. In patients with LLD, higher vascular burden, but not tau, was associated with lower MTL volume and more pronounced WM differences.

LLD was associated with both GM and WM differences in the MTL. Cerebrovascular disease, rather than AD type tau-mediated neurodegenerative processes, may contribute to brain tissue differences in LLD.