Deep brain stimulation (DBS) is an effective treatment for Parkinson’s disease but can be complicated by side-effects such as cognitive decline. There is often a delay before this side-effect is apparent and the mechanism is unknown, making it difficult to identify patients at risk or select appropriate DBS settings. Here, we test whether connectivity between the stimulation site and other brain regions is associated with cognitive decline following DBS. First, we studied a unique patient cohort with cognitive decline following subthalamic DBS for Parkinson’s disease (n = 10) where re-programming relieved the side-effect without loss of motor benefit. Using resting state functional connectivity data from a large normative cohort (n = 1000), we computed connectivity between each stimulation site and the subiculum, an a priori brain region functionally connected to brain lesions causing memory impairment. Connectivity between DBS sites and this same subiculum region was significantly associated with DBS induced cognitive decline (P < 0.02). We next performed a data-driven analysis to identify connnections most associated with DBS induced cognitive decline. DBS sites causing cognitive decline (versus those that did not) were more connected to the anterior cingulate, caudate nucleus, hippocampus, and cognitive regions of the cerebellum (Pfwe< 0.05). The spatial topography of this DBS-based circuit for cognitive decline aligned with an a priori lesion-based circuit for memory impairment (P = 0.017). To begin translating these results into a clinical tool that might be used for DBS programming, we generated a “heatmap” in which the intensity of each voxel reflects the connectivity to our cognitive decline circuit. We then validated this heatmap using an independent dataset of PD patients in which cognitive performance was measured following subthalamic DBS (n = 33). Intersection of DBS sites with our heatmap was correlated with changes in the Mattis dementia rating scale one year after lead implantation (r = 0.39; p = 0.028). Finally, to illustrate how this heatmap might be used in clinical practice, we present a case that was flagged as “high risk” for cognitive decline based on intersection of the patient’s DBS site with our heatmap. This patient had indeed experienced cognitive decline and our heatmap was used to select alternative DBS parameters. At 14 days follow-up the patient’s cognition improved without loss of motor benefit. These results lend insight into the mechanism of DBS induced cognitive decline and suggest that connectivity-based heatmaps may help identify patients at risk and who might benefit from DBS reprogramming.