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Dickerson, Bradford

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Dickerson, Bradford
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    Alzheimer's-Related Cortical Atrophy Is Associated With Postoperative Delirium Severity in Persons Without Dementia
    (Elsevier BV, 2017-11) Racine, Annie M.; Fong, Tamara; Travison, Thomas; Jones, Richard N.; Gou, Yun; Vasunilashorn, Sarinnapha; Marcantonio, Edward; Alsop, David; Inouye, Sharon; Dickerson, Bradford
    Patients with dementia due to Alzheimer’s disease (AD) have increased risk of developing delirium. This study investigated the relationship between a magnetic resonance imaging (MRI)-derived biomarker associated with preclinical AD and postoperative delirium. Participants were older adults (≥70 years) without dementia who underwent preoperative MRI and elective surgery. Delirium incidence and severity were evaluated daily during hospitalization. Cortical thickness was averaged across a published set of a priori brain regions to derive a measure known as the “AD signature.” Logistic and linear regression was used, respectively, to test whether the AD signature was associated with delirium incidence in the entire sample (N=145) or with the severity of delirium among those who developed delirium (N=32). Thinner cortex in the AD signature did not predict incidence of delirium (odds ratio=1.15, p=.38), but was associated with greater delirium severity among those who developed delirium (b=−1.2, p=.014). These results suggest that thinner cortices, perhaps reflecting underlying neurodegeneration due to preclinical AD, may serve as a vulnerability factor that increases severity once delirium occurs.
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    Consensus classification of posterior cortical atrophy
    (2017) Crutch, Sebastian J.; Schott, Jonathan M.; Rabinovici, Gil D.; Murray, Melissa; Snowden, Julie S.; van der Flier, Wiesje M.; Dickerson, Bradford; Vandenberghe, Rik; Ahmed, Samrah; Bak, Thomas H.; Boeve, Bradley F.; Butler, Christopher; Cappa, Stefano F.; Ceccaldi, Mathieu; de Souza, Leonardo Cruz; Dubois, Bruno; Felician, Olivier; Galasko, Douglas; Graff-Radford, Jonathan; Graff-Radford, Neill R.; Hof, Patrick R.; Krolak-Salmon, Pierre; Lehmann, Manja; Magnin, Eloi; Mendez, Mario F.; Nestor, Peter J.; Onyike, Chiadi U.; Pelak, Victoria S.; Pijnenburg, Yolande; Primativo, Silvia; Rossor, Martin N.; Ryan, Natalie S.; Scheltens, Philip; Shakespeare, Timothy J.; González, Aida Suárez; Tang-Wai, David F.; Yong, Keir X. X.; Carrillo, Maria; Fox, Nick C.
    Introduction: A classification framework for posterior cortical atrophy (PCA) is proposed to improve the uniformity of definition of the syndrome in a variety of research settings. Methods: Consensus statements about PCA were developed through a detailed literature review, the formation of an international multidisciplinary working party which convened on four occasions, and a Web-based quantitative survey regarding symptom frequency and the conceptualization of PCA. Results: A three-level classification framework for PCA is described comprising both syndrome- and disease-level descriptions. Classification level 1 (PCA) defines the core clinical, cognitive, and neuroimaging features and exclusion criteria of the clinico-radiological syndrome. Classification level 2 (PCA-pure, PCA-plus) establishes whether, in addition to the core PCA syndrome, the core features of any other neurodegenerative syndromes are present. Classification level 3 (PCA attributable to AD [PCA-AD], Lewy body disease [PCA-LBD], corticobasal degeneration [PCA-CBD], prion disease [PCA-prion]) provides a more formal determination of the underlying cause of the PCA syndrome, based on available pathophysiological biomarker evidence. The issue of additional syndrome-level descriptors is discussed in relation to the challenges of defining stages of syndrome severity and characterizing phenotypic heterogeneity within the PCA spectrum. Discussion There was strong agreement regarding the definition of the core clinico-radiological syndrome, meaning that the current consensus statement should be regarded as a refinement, development, and extension of previous single-center PCA criteria rather than any wholesale alteration or redescription of the syndrome. The framework and terminology may facilitate the interpretation of research data across studies, be applicable across a broad range of research scenarios (e.g., behavioral interventions, pharmacological trials), and provide a foundation for future collaborative work.
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    Cortical thickness and subcortical brain volumes in professional rugby league players
    (Elsevier, 2018) Wojtowicz, Magdalena; Gardner, Andrew J.; Stanwell, Peter; Zafonte, Ross; Dickerson, Bradford; Iverson, Grant
    Purpose The purpose of this study was to examine cortical thickness and subcortical volumes in professional rugby players with an extensive history of concussions compared to control subjects. Method Participants included 24 active and former professional rugby league players [Age M(SD) = 33.3(6.3); Range = 21–44] with an extensive history of concussion and 18 age- and education-matched controls with no history of neurotrauma or participation in contact sports. Participants underwent T1-weighted imaging and completed a neuropsychological battery, including two tests of memory. Whole brain cortical thickness analysis and structural volume analysis was performed using FreeSurfer version 6.0. Results: Professional rugby league players reported greater alcohol consumption (p < .001) and had significantly worse delayed recall of a visually complex design (p = .04). They did not differ from controls on other clinical outcome measures. There were no differences in cortical thickness between the groups. Professional players had smaller whole brain (p = .003), bilateral hippocampi (ps = .03), and left amygdala volumes (p = .01) compared to healthy controls. Within the players group, there were significant associations between greater alcohol use and smaller bilateral hippocampi and left amygdala volumes. There were no associations between structural volumes and history of concussions or memory performance. Conclusions: The literature examining cortical thickness in athletes with a history of multiple concussions is mixed. We did not observe differences in cortical thickness in professional rugby league players compared to controls. However, smaller subcortical volumes were found in players that were, in part, associated with greater alcohol consumption.
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    Impaired memory is more closely associated with brain beta-amyloid than leukoaraiosis in hypertensive patients with cognitive symptoms
    (Public Library of Science, 2018) Smith, Eric E.; Muzikansky, Alona; McCreary, Cheryl R.; Batool, Saima; Viswanathan, Anand; Dickerson, Bradford; Johnson, Keith; Greenberg, Steven; Blacker, Deborah
    Background: Hypertension is the strongest modifiable risk factor for subcortical ischemic changes and is also a risk factor for Alzheimer’s dementia. We used neuroimaging to investigate the pathological basis of early cognitive symptoms in patients with hypertension. Methods: In this cross-sectional cohort study 67 patients age >60 years with hypertension and Clinical Dementia Rating scale score of 0.5 without dementia, and without history of symptomatic stroke, underwent MRI for measurement of subcortical vascular changes and positron emission tomography (PET) scan with Pittsburgh Compound B (PiB-PET) to detect beta-amyloid deposition. These imaging measures were related to neuropsychological tests of memory, executive function and processing speed. Results: Mean age was 75.0 (standard deviation, SD, 7.3). Mean neuropsychological Z scores were: episodic memory -0.63 (SD 1.23), executive function -0.40 (SD 1.10), processing speed -0.24 (SD 0.88); 22 of the 67 subjects met criteria for mild cognitive impairment (MCI) and the remaining 45 subjects had subjective cognitive concerns only. In multivariable models adjusting for age and years of education, each 0.1 unit increase in mean cortical PiB-PET binding was associated with 0.14 lower mean Z score for episodic memory (95% CI -0.28 to -0.01). This means that for every 0.1 unit increase in mean cortical PiB-PET, episodic memory was 0.14 standard deviations lower. White matter hyperintensity volume, silent brain infarcts and microbleeds were not associated with neuropsychological test scores. Conclusions: Episodic memory was prominently affected in hypertensive participants with MCI or subjective cognitive concerns, and was associated with PiB-PET binding. This suggests a prominent role for Alzheimer pathology in cognitive impairment even in hypertensive participants at elevated risk for vascular cognitive impairment.
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    The personalized Alzheimer's disease cortical thickness index predicts likely pathology and clinical progression in mild cognitive impairment
    (Elsevier, 2018) Racine, Annie M.; Brickhouse, Michael; Wolk, David A.; Dickerson, Bradford
    Introduction: An Alzheimer's disease (AD) biomarker adjusted for age-related brain changes should improve specificity for AD-related pathological burden. Methods: We calculated a brain-age-adjusted “personalized AD cortical thickness index” (pADi) in mild cognitive impairment patients from the Alzheimer's Disease Neuroimaging Initiative. We performed receiver operating characteristic analysis for discrimination between patients with and without cerebrospinal fluid evidence of AD and logistic regression in an independent sample to determine if a dichotomized pADi predicted conversion to AD dementia. Results: Receiver operating characteristic area under the curve was 0.69 and 0.72 in the two samples. Three empirical methods identified the same cut-point for pADi in the discovery sample. In the validation sample, 83% of pADi+ mild cognitive impairment patients were cerebrospinal fluid AD biomarker positive. pADi+ mild cognitive impairment patients (n = 63, 38%) were more likely to progress to AD dementia after 1 (odds ratio = 2.9) and 3 (odds ratio = 2.6) years. Discussion The pADi is a personalized, magnetic resonance imaging–derived AD biomarker that predicts progression to dementia.
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    Evidence for a Large-Scale Brain System Supporting Allostasis and Interoception in Humans
    (2017) Kleckner, Ian R.; Zhang, Jiahe; Touroutoglou, Alexandra; Chanes, Lorena; Xia, Chenjie; Simmons, W. Kyle; Quigley, Karen S.; Dickerson, Bradford; Barrett, Lisa Feldman
    Large-scale intrinsic brain systems have been identified for exteroceptive senses (e.g., sight, hearing, touch). We introduce an analogous system for representing sensations from within the body, called interoception, and demonstrate its relation to regulating peripheral systems in the body, called allostasis. Employing the recently introduced Embodied Predictive Interoception Coding (EPIC) model, we used tract-tracing studies of macaque monkeys, followed by two intrinsic functional magnetic resonance imaging samples (N = 280 and N = 270) to evaluate the existence of an intrinsic allostatic/interoceptive system in the human brain. Another sample (N = 41) allowed us to evaluate the convergent validity of the hypothesized allostatic/interoceptive system by showing that individuals with stronger connectivity between system hubs performed better on an implicit index of interoceptive ability related to autonomic fluctuations. Implications include insights for the brain’s functional architecture, dissolving the artificial boundary between mind and body, and unifying mental and physical illness.
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    Does amyloid deposition produce a specific atrophic signature in cognitively normal subjects?☆
    (Elsevier, 2013) Whitwell, Jennifer L.; Tosakulwong, Nirubol; Weigand, Stephen D.; Senjem, Matthew L.; Lowe, Val J.; Gunter, Jeffrey L.; Boeve, Bradley F.; Knopman, David S.; Dickerson, Bradford; Petersen, Ronald C.; Jack, Clifford R.
    The objective of our study was to evaluate whether cognitively normal (CN) elderly participants showing elevated cortical beta-amyloid (Aβ) deposition have a consistent neuroanatomical signature of brain atrophy that may characterize preclinical Alzheimer's disease (AD). 115 CN participants who were Aβ-positive (CN +) by amyloid PET imaging; 115 CN participants who were Aβ-negative (CN −); and 88 Aβ-positive mild cognitive impairment or AD participants (MCI/AD +) were identified. Cortical thickness (FreeSurfer) and gray matter volume (SPM5) were measured for 28 regions-of-interest (ROIs) across the brain and compared across groups. ROIs that best discriminated CN − from CN + differed for FreeSurfer cortical thickness and SPM5 gray matter volume. Group-wise discrimination was poor with a high degree of uncertainty in terms of the rank ordering of ROIs. In contrast, both techniques showed strong and consistent findings comparing MCI/AD + to both CN − and CN + groups, with entorhinal cortex, middle and inferior temporal lobe, inferior parietal lobe, and hippocampus providing the best discrimination for both techniques. Concordance across techniques was higher for the CN − and CN + versus MCI/AD + comparisons, compared to the CN − versus CN + comparison. The weak and inconsistent nature of the findings across technique in this study cast doubt on the existence of a reliable neuroanatomical signature of preclinical AD in elderly PiB-positive CN participants.
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    Biomarker-based prediction of progression in MCI: Comparison of AD signature and hippocampal volume with spinal fluid amyloid-β and tau
    (Frontiers Media S.A., 2013) Dickerson, Bradford; Wolk, David A.
    Objective: New diagnostic criteria for mild cognitive impairment (MCI) due to Alzheimer's disease (AD) have been developed using biomarkers aiming to establish whether the clinical syndrome is likely due to underlying AD. We investigated the utility of magnetic resonance imaging (MRI) and cerebrospinal fluid (CSF) biomarkers in predicting progression from amnesic MCI to dementia, testing the hypotheses that (1) markers of amyloid and neurodegeneration provide distinct and complementary prognostic information over different time intervals, and that (2) evidence of neurodegeneration in amyloid-negative MCI individuals would be useful prognostically. Methods: Data were obtained from the ADNI-1 (Alzheimer's Disease Neuroimaging Initiative Phase 1) database on all individuals with a baseline diagnosis of MCI, baseline MRI and CSF data, and at least one follow-up visit. MRI data were processed using a published set of a priori regions of interest to derive a measure known as the ``AD signature,'' as well as hippocampal volume. The CSF biomarkers amyloid-β, total tau, and phospho tau were also examined. We performed logistic regression analyses to identify the best baseline biomarker predictors of progression to dementia over 1 or 3 years, and Cox regression models to test the utility of these markers for predicting time-to-dementia. Results: For prediction of dementia in MCI, the AD signature cortical thickness biomarker performed better than hippocampal volume. Although CSF tau measures were better than CSF amyloid-β at predicting dementia within 1 year, the AD signature was better than all CSF measures at prediction over this relatively short-term interval. CSF amyloid-β was superior to tau and AD signature at predicting dementia over 3 years. When CSF amyloid-β was dichotomized using previously published cutoff values and treated as a categorical variable, a multivariate stepwise Cox regression model indicated that both the AD signature MRI marker and the categorical CSF amyloid-β marker were useful in predicting time-to-event diagnosis of AD dementia. Conclusion: In amnesic MCI, short-term (1 year) prognosis of progression to dementia relates strongly to baseline markers of neurodegeneration, with the AD signature MRI biomarker of cortical thickness performing the best among MRI and CSF markers studied here. Longer-term (3 year) prognosis in these individuals was better predicted by a marker indicative of brain amyloid. Prediction of time-to-event in a survival model was predicted by the combination of these biomarkers. These results provide further support for emerging models of the temporal relationship of pathophysiologic events in AD and demonstrate the utility of these biomarkers at the prodromal stage of the illness.
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    Fluid intelligence and brain functional organization in aging yoga and meditation practitioners
    (Frontiers Media S.A., 2014) Gard, Tim; Taquet, Maxime; Dixit, Rohan; Hölzel, Britta K.; de Montjoye, Yves-Alexandre; Brach, Narayan; Salat, David; Dickerson, Bradford; Gray, Jeremy R.; Lazar, Sara
    Numerous studies have documented the normal age-related decline of neural structure, function, and cognitive performance. Preliminary evidence suggests that meditation may reduce decline in specific cognitive domains and in brain structure. Here we extended this research by investigating the relation between age and fluid intelligence and resting state brain functional network architecture using graph theory, in middle-aged yoga and meditation practitioners, and matched controls. Fluid intelligence declined slower in yoga practitioners and meditators combined than in controls. Resting state functional networks of yoga practitioners and meditators combined were more integrated and more resilient to damage than those of controls. Furthermore, mindfulness was positively correlated with fluid intelligence, resilience, and global network efficiency. These findings reveal the possibility to increase resilience and to slow the decline of fluid intelligence and brain functional architecture and suggest that mindfulness plays a mechanistic role in this preservation.
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    Resting connectivity between salience nodes predicts recognition memory
    (Oxford University Press, 2017) Andreano, Joseph M.; Touroutoglou, Alexandra; Dickerson, Bradford; Barrett, Lisa F.
    Abstract The resting connectivity of the brain’s salience network, particularly the ventral subsystem of the salience network, has been previously associated with various measures of affective reactivity. Numerous studies have demonstrated that increased affective arousal leads to enhanced consolidation of memory. This suggests that individuals with greater ventral salience network connectivity will exhibit greater responses to affective experience, leading to a greater enhancement of memory by affect. To test this hypothesis, resting ventral salience connectivity was measured in 41 young adults, who were then exposed to neutral and negative affect inductions during a paired associate memory test. Memory performance for material learned under both negative and neutral induction was tested for correlation with resting connectivity between major ventral salience nodes. The results showed a significant interaction between mood induction (negative vs neutral) and connectivity between ventral anterior insula and pregenual anterior cingulate cortex, indicating that salience node connectivity predicted memory for material encoded under negative, but not neutral induction. These findings suggest that the network state of the perceiver, measured prior to affective experience, meaningfully influences the extent to which affect modulates memory. Implications of these findings for individuals with affective disorder, who show alterations in both connectivity and memory, are considered.