Early alcohol initiation is associated with higher lifetime Parkinson's disease risk after accounting for exposure latency.

Poststroke depression is the most prevalent psychological condition after stroke, affecting about one‐third of survivors. Patients with poststroke depression face greater risk of poor recovery, recurrent stroke, reduced quality of life, and higher mortality than those without depression., , Given the profound individual and societal impact of poststroke depression, accurate identification of vulnerability to depression after stroke is vital. Characterizing the neural underpinnings of poststroke depression is key to understanding it and predicting those at a higher risk; enabling targeted treatment, improved prognosis, better quality of life, and potentially reducing healthcare costs. Despite many attempts to elucidate the mechanisms of poststroke depression, identifying robust neural predictors has proven challenging. Recent work has argued against a strong role for lesion location: Padmanabhan et al., for example, found that focal lesions alone did not significantly predict depression, whereas lesion locations associated with depressive symptoms were functionally connected to a shared network centered on the left dorsolateral prefrontal cortex. These findings align with network‐based models proposing that depression arises from dysfunctional processing within specific networks, including the frontostriatal network., However, the literature on focal lesion correlates of poststroke depression is more mixed than often acknowledged. At least three voxel‐based lesion‐symptom mapping (VLSM) studies have reported associations between poststroke depression and focal lesions in regions such as the basal ganglia and dorsolateral prefrontal cortex., , These studies suggest that discrete lesion locations may contribute to vulnerability to depression, underscoring the need to integrate both focal and network‐level perspectives when interpreting neural predictors of poststroke mood outcomes.