Biology subjects

Berman, S. E.

Publications and source records attributed to Berman, S. E..

3 recordsLinked to original sources

bioRxiv2019

Adolescent substance use and functional connectivity between the ventral striatum and hippocampus

Neurodevelopmental explanations for adolescent substance use have focused on heightened sensitivity of the brains reward system, centered around the ventral striatum (VS). Recent evidence demonstrates increased functional connectivity between the VS and hippocampus in adolescents relative to adults, suggesting that the adolescent brain may learn from subsequent exposure to risks/rewards. However, a link between VS-hippocampal circuitry and adolescent substance use has yet to be established. Two separate longitudinal studies were conducted to evaluate whether variation in VS-hippocampal resting-state functional connectivity (rs-FC) predicts subsequent adolescent substance use. Study 1 consisted of 19 youth recruited from a high sociodemographic risk population (N = 19; 14 female; 47% Black Non-Hispanic, 32% White Non-Hispanic). To replicate results of Study 1, Study 2 utilized data from the National Consortium on Adolescent Neurodevelopment and Alcohol, an ongoing multi-site imaging study (N= 644; 339 female; 11% Black Non-Hispanic, 11% Hispanic/Latino, 66% White Non-Hispanic). Resting-state fMRI data were collected at a baseline time point and lifetime and past year self-reported substance use was collected at a follow up visit. Regression models tested whether baseline VS-hippocampal rs-FC predicted substance use at follow up. Across both studies, higher VS-hippocampal rs-FC at baseline predicted greater substance use at follow up. These data provide the first evidence linking increased VS-hippocampal connectivity with greater adolescent substance use. Results fit with the emerging idea that adolescent substance use is driven by not only a heightened sensitivity to reward, but also a stronger link between reinforcement learning and episodic memory for rewarding outcomes.

neuroscience↗

bioRxiv2017

Modifiable risk factors moderate the relationship between amyloid and cognition in midlife

Although evidence suggests a relationship between elevated beta-amyloid and cognitive decline, approximately 30% of older adults with positive markers of amyloid remain cognitively healthy. Our objective was to test if the presence of modifiable risk factors (i.e., central obesity, hypertension, and depressive symptoms) moderated the relationship between amyloid and longitudinal cognitive performance. Data were from 207 adults (140 females; age range=40-70) enriched for Alzheimers disease risk (73% parental history of Alzheimers disease) enrolled in the Wisconsin Registry for Alzheimers Prevention study. Participants completed at least two neuropsychological evaluations and one biomarker visit ([C11] Pittsburgh Compound B PET scan or lumbar puncture). Participants were characterized as high or low on amyloid using cutoffs developed for [C11] Pittsburgh Compound B-PET distribution volume ratio or CSF amyloid beta 1-42 values. Participants were also coded as high or low risk on obesity, hypertension, and depressive symptoms. Linear mixed effects regression models examined three-way interactions between modifiable risk factor status x amyloid group x age at each study visit on longitudinal Verbal Learning & Memory and Speed & Flexibility factor scores. Results indicated that the relationship between beta-amyloid and Verbal Learning & Memory decline was associated with hypertension status (Likelihood ratio test for significance of hypertension status age x amyloid status x visit age interaction term;{chi} 2 (1) = 5.28, p = .02). The relationship between beta-amyloid and Speed & Flexibility decline was associated with depression status (Likelihood ratio test for significance of amyloid status x depression status x visit age interaction term;{chi} 2 (1) = 7.10, p = .03). The presence of obesity did not significantly moderate the relationship between beta-amyloid status and cognitive performance, although the direction of relationship was similar to above relationships (Likelihood ratio test for significance of obesity status x amyloid status x visit age interaction term;{chi} 2 (1) = 1.52, p = .21). In this at-risk for Alzheimers disease cohort, the modifiable risk factors of hypertension and depression significantly moderated the relationship between beta-amyloid and cognitive decline. Identification and modification of these risk factors in late middle age may slow the effect of amyloid on the progression of cognitive symptoms.

neuroscience↗

bioRxiv2017

The Wisconsin Registry for Alzheimer’s Prevention: A Review of findings and current directions

The Wisconsin Registry for Alzheimers Prevention (WRAP) is a longitudinal observational cohort study enriched with persons with a parental history (PH) of probable Alzheimers Disease (AD) dementia. Since late 2001, WRAP has enrolled 1,561 people at a mean baseline age of 54. Participants return for a second visit four years after baseline and subsequent visits occur every two years. Eighty-one percent (1270) of participants remain active in the study at a current mean age of 64 and 9 years of follow-up. Serially assessed cognition, self-reported medical and lifestyle histories (e.g. diet, physical and cognitive activity, sleep, and mood), laboratory tests, genetics, and linked studies comprising molecular imaging, structural imaging and cerebrospinal fluid data, have yielded many important findings. In this cohort, PH of probable AD is associated with 46% APOE {varepsilon}4 positivity, more than twice the rate of 22% among persons without PH. Subclinical or worse cognitive decline relative to internal normative data has been observed in 17.6% of the cohort. Twenty-eight percent exhibit amyloid and/or tau positivity. Biomarker elevations, but not APOE or PH status, are associated with cognitive decline. Salutary health and lifestyle factors are associated with better cognition and brain structure, and lower AD pathophysiologic burden. Of paramount importance is establishing the amyloid and tau AD endophenotypes to which cognitive outcomes can be linked. Such data will provide new knowledge on the early temporal course of AD pathophysiology and inform the design of secondary prevention clinical trials.

neuroscience↗