Although manganese (Mn) is a trace metal essential for humans, chronic exposure to Mn can cause accumulation of this metal ion in the brain leading to an increased risk of neurological and neurobehavioral health effects. This is a concern for welders exposed to Mn through welding fumes. While brain Mn accumulation in occupational settings has mostly been reported in the basal ganglia, several imaging studies also revealed elevated Mn in other brain areas. Since Mn functions as a magnetic resonance imaging (MRI) T1 contrast agent, we developed a whole-brain MRI approach to map in vivo Mn deposition differences in the brains of non-exposed factory controls and exposed welders. This is a cross-sectional analysis of 23 non-exposed factory controls and 36 exposed full-time welders from the same truck manufacturer. We collected high-resolution 3D MRIs of brain anatomy and R1 relaxation maps to identify regional differences using voxel-based quantification (VBQ) and statistical parametric mapping. Furthermore, we investigated the associations between excess Mn deposition and neuropsychological and motor test performance. Our results indicate that: (1) Using whole-brain MRI relaxometry methods we can generate excess Mn deposition maps in vivo, (2) excess Mn accumulation due to occupational exposure occurs beyond the basal ganglia in cortical areas associated with motor and cognitive functions, (3) Mn likely diffuses along white matter tracts in the brain, and (4) Mn deposition in specific brain regions is associated with exposure (cerebellum and frontal cortex) and motor metrics (cerebellum and hippocampus).

Limited research suggests mushroom consumption may improve indexes of brain health. Mushrooms contain bioactive compounds and antioxidants capable of crossing the blood–brain barrier and impacting vital neurological processes. We conducted a randomized controlled feeding trial assessing the effects of adopting a healthy U.S. Mediterranean-style dietary pattern (MED) with or without mushrooms on indexes of brain health and well-being. Sixty adults (aged 46 ± 12 y; BMI 28.3 ± 2.84 kg/m²; mean ± SD) without severe depression consumed a fully controlled MED diet with 84 g/d of mushrooms (4 d/week white button and 3 d/week oyster) or without (control with breadcrumbs) for 8 weeks. At baseline and post-intervention, surveys were used to evaluate anxiety, depression, mood, and well-being, and behavioral tests were used to evaluate cognition. Consumption of the MED diet, with or without mushrooms, increased (improved) self-reported vigor/activity (Time p = 0.026) and both behavioral measures of immediate memory (Time p < 0.05). Mixed effects were observed for other domains of neuropsychological function, and there were no changes in other measured indexes of brain health with the consumption of either MED diet. Adopting a healthy MED-style dietary pattern, with or without consuming white button and oyster mushrooms, may improve vigor/activity and immediate memory among middle-aged and older adults.

The etiological heterogeneity of depression poses a challenge for prevention and intervention efforts. One solution is to map unique etiological pathways for subgroups defined by a singular risk factor. A relevant population for this approach is women who carry the premutation of the fragile X messenger ribonucleoprotein 1 (FMR1) gene, who are at high risk for adult-onset depression. This study explores a candidate neurophysiological marker of depression risk: reduced reward sensitivity, indexed by the reward positivity (RewP). The RewP has been linked to depression risk in the general population, but is unexplored within FMR1 premutation carriers. 16 women with the FMR1 premutation and a matched control group completed a simple guessing task while the electroencephalogram was recorded. Among premutation carriers, RewP difference score (win versus loss) was reduced. These preliminary finding suggest that the FMR1 premutation may confer increased risk for depression in part through abnormal neural sensitivity to rewards.

The FMR1 premutation is associated with a complex clinical phenotype, with increased risk for outcomes across the domains of psychological disorders, motor functioning, and reproductive health. A key gap is understanding intermediate processing that may help to explain how the FMR1 premutation alters brain functioning to confer increased risk across these domains. The current study begins to address this gap by focusing on two candidate, interrelated processes: cerebellar GABA and executive function. Data were collected from a cohort of 15 adult female FMR1 premutation carriers and a comparison group of 15 age-matched unaffected controls. Cerebellar GABA concentration was measured using edited magnetic resonance spectroscopy (MEGA-sLASER) at 3 T. Executive function was measured across two units of analysis: the error-related negativity, an EEG marker of automatic error detection, as well as performance-based measures from validated neuropsychological tests. Premutation carriers exhibited an atypical scalp topography of the error-related negativity. In controls but not in premutation carriers, error-related brain activity was associated with cerebellar GABA concentration and performance-based executive function. This pattern of preliminary findings suggests that the FMR1 premutation may alter the neural network involved in error monitoring. If these findings are confirmed in larger cohorts, they have potential implications for understanding the emergence of the broader clinical phenotype in adult FMR1 premutation carriers.