The concept of subjective value is central to current neurobiological views of economic decision-making. Much of this work has focused on signals in the ventromedial frontal lobe (VMF) that correlate with the subjective value of a variety of stimuli (e.g., food, monetary gambles), and are thought to support decision-making. However, the neural processes involved in assessing and integrating value information from the attributes of such complex options remain to be defined. Here, we tested the necessary role of VMF in weighting attributes of naturalistic stimuli during value judgments. We asked how distinct attributes of visual artworks influenced the subjective value ratings of subjects with VMF damage, compared to healthy participants and a frontal lobe damaged control group. Subjects with VMF damage were less influenced by the energy (emotion, complexity) and color radiance (warmth, saturation) of the artwork, while they were similar to control groups in considering saliency, balance and concreteness. These dissociations argue that VMF is critical for allowing certain affective content to influence subjective value, while sparing the influence of perceptual or representational information. These distinctions are important for better defining the often-underspecified concept of subjective value and developing more detailed models of the brain mechanisms underlying decision behavior.

Objective To investigate the relationship between the topography of amyloid‐β plaques, tau neurofibrillary tangles, and the overlap between the two, with cognitive dysfunction in individuals without dementia. Methods We evaluated 154 individuals who were assessed with amyloid‐β PET with [18F]AZD4694, tau‐PET with [18F]MK6240, structural MRI, and neuropsychological testing. We also evaluated an independent cohort of 240 individuals who were assessed with amyloid‐β PET with [18F]Florbetapir, tau‐PET with [18F]Flortaucipir, structural MRI, and neuropsychological testing. Using the VoxelStats toolbox, we conducted voxel‐wise linear regressions between amyloid‐PET, tau‐PET, and their interaction with cognitive function, correcting for age, sex, and years of education. Results In both cohorts, we observed that tau‐PET standardized uptake value ratio in medial temporal lobes was associated with clinical dementia rating Sum of Boxes (CDR‐SoB) scores independently of local amyloid‐PET uptake (FWE corrected at p < 0.001). We also observed in both cohorts that in regions of the neocortex, associations between neocortical tau‐PET and clinical function were dependent on local amyloid‐PET (FWE corrected at p < 0.001). Interpretation In medial temporal brain regions, characterized by the accumulation of tau pathology in the absence of amyloid‐β, tau had direct associations with cognitive dysfunction. In brain regions characterized by the accumulation of both amyloid‐β and tau pathologies such as the posterior cingulate and medial frontal cortices, tau’s relationship with cognitive dysfunction was dependent on local amyloid‐β concentrations. Our results provide evidence that amyloid‐β in Alzheimer’s disease influences cognition by potentiating the deleterious effects of tau pathology.

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