N. Maritza Dowling
University of Wisconsin-Madison
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Featured researches published by N. Maritza Dowling.
Review of Educational Research | 2008
Geoffrey D. Borman; N. Maritza Dowling
This comprehensive meta-analysis on teacher career trajectories, consisting of 34 studies of 63 attrition moderators, seeks to understand why teaching attrition occurs, or what factors moderate attrition outcomes. Personal characteristics of teachers are important predictors of turnover. Attributes of teachers’ schools, including organizational characteristics, student body composition, and resources (instructional spending and teacher salaries), are also key moderators. The evidence suggests that attrition from teaching is (a) not necessarily “healthy” turnover, (b) influenced by various personal and professional factors that change across teachers’ career paths, (c) more strongly moderated by characteristics of teachers’ work conditions than previously noted in the literature, and (d) a problem that can be addressed through policies and initiatives. Though researchers have utilized a number of national and state databases and have applied economic labor theory to questions related to teacher attrition, the authors argue that better longitudinal data on teacher career paths and more nuanced theories are needed.
PLOS Medicine | 2015
Carey E. Gleason; N. Maritza Dowling; Whitney Wharton; JoAnn E. Manson; Virginia M. Miller; Craig S. Atwood; Eliot A. Brinton; Marcelle I. Cedars; Rogerio A. Lobo; Genevieve Neal-Perry; Nanette Santoro; Hugh S. Taylor; Dennis M. Black; Matthew J. Budoff; Howard N. Hodis; Frederick Naftolin; S. Mitchell Harman; Sanjay Asthana
Background Menopausal hormone therapy (MHT) reportedly increases the risk of cognitive decline in women over age 65 y. It is unknown whether similar risks exist for recently postmenopausal women, and whether MHT affects mood in younger women. The ancillary Cognitive and Affective Study (KEEPS-Cog) of the Kronos Early Estrogen Prevention Study (KEEPS) examined the effects of up to 4 y of MHT on cognition and mood in recently postmenopausal women. Methods and Findings KEEPS, a randomized, double-blinded, placebo-controlled clinical trial, was conducted at nine US academic centers. Of the 727 women enrolled in KEEPS, 693 (95.3%) participated in the ancillary KEEPS-Cog, with 220 women randomized to receive 4 y of 0.45 mg/d oral conjugated equine estrogens (o-CEE) plus 200 mg/d micronized progesterone (m-P) for the first 12 d of each month, 211 women randomized to receive 50 μg/d transdermal estradiol (t-E2) plus 200 mg/d m-P for the first 12 d of each month, and 262 women randomized to receive placebo pills and patches. Primary outcomes included the Modified Mini-Mental State examination; four cognitive factors: verbal learning/memory, auditory attention/working memory, visual attention/executive function, and speeded language/mental flexibility; and a mood measure, the Profile of Mood States (POMS). MHT effects were analyzed using linear mixed-effects (LME) models, which make full use of all available data from each participant, including those with missing data. Data from those with and without full data were compared to assess for potential biases resulting from missing observations. For statistically significant results, we calculated effect sizes (ESs) to evaluate the magnitude of changes. On average, participants were 52.6 y old, and 1.4 y past their last menstrual period. By month 48, 169 (24.4%) and 158 (22.8%) of the 693 women who consented for ancillary KEEPS-Cog were lost to follow-up for cognitive assessment (3MS and cognitive factors) and mood evaluations (POMS), respectively. However, because LME models make full use all available data, including data from women with missing data, 95.5% of participants were included in the final analysis (n = 662 in cognitive analyses, and n = 661 in mood analyses). To be included in analyses, women must have provided baseline data, and data from at least one post-baseline visit. The mean length of follow-up was 2.85 y (standard deviation [SD] = 0.49) for cognitive outcomes and 2.76 (SD = 0.57) for mood outcomes. No treatment-related benefits were found on cognitive outcomes. For mood, model estimates indicated that women treated with o-CEE showed improvements in depression and anxiety symptoms over the 48 mo of treatment, compared to women on placebo. The model estimate for the depression subscale was −5.36 × 10−2 (95% CI, −8.27 × 10−2 to −2.44 × 10−2; ES = 0.49, p < 0.001) and for the anxiety subscale was −3.01 × 10−2 (95% CI, −5.09 × 10−2 to −9.34 × 10−3; ES = 0.26, p < 0.001). Mood outcomes for women randomized to t-E2 were similar to those for women on placebo. Importantly, the KEEPS-Cog results cannot be extrapolated to treatment longer than 4 y. Conclusions The KEEPS-Cog findings suggest that for recently postmenopausal women, MHT did not alter cognition as hypothesized. However, beneficial mood effects with small to medium ESs were noted with 4 y of o-CEE, but not with 4 y of t-E2. The generalizability of these findings is limited to recently postmenopausal women with low cardiovascular risk profiles. Trial Registration ClinicalTrials.gov NCT00154180 and NCT00623311
Educational Evaluation and Policy Analysis | 2006
Geoffrey D. Borman; N. Maritza Dowling
Employing a randomized field trial, this 3-year study explored the effects of a multiyear summer school program in preventing the cumulative effect of summer learning losses and promoting longitudinal achievement growth, for a total treatment group of 438 students from high-poverty schools. Longitudinal outcomes for the participants were contrasted to those for 248 children randomized into a no-treatment control condition. Multilevel growth models revealed no intention-to-treat effects of assignment to the multiyear summer school program. However, student attendance patterns at the voluntary program were variable across the 3 years that the intervention was offered. Maximum likelihood mixture models, which estimated the effects of the treatment for compliers, revealed statistically significant effects on learning across all three literacy domains tested for those students who attended the Summer Academy at an above average rate across two or more of the three summers that it was offered. Relative to their control-group counterparts, treatment compliers held advantages of 40% to 50% of one grade level on the final posttests.
Neurobiology of Aging | 2014
Sterling C. Johnson; Bradley T. Christian; Ozioma C. Okonkwo; Jennifer M. Oh; Sandra Harding; Guofan Xu; Ansel T. Hillmer; Dustin Wooten; Dhanabalan Murali; Todd E. Barnhart; Lance Hall; Annie M. Racine; William E. Klunk; Chester A. Mathis; Barbara B. Bendlin; Catherine L. Gallagher; Cynthia M. Carlsson; Howard A. Rowley; Bruce P. Hermann; N. Maritza Dowling; Sanjay Asthana; Mark A. Sager
To determine the relationship between amyloid burden and neural function in healthy adults at risk for Alzheimers Disease (AD), we used multimodal imaging with [C-11]Pittsburgh compound B positron emission tomography, [F-18]fluorodeoxyglucose, positron emission tomography , and magnetic resonance imaging, together with cognitive measurement in 201 subjects (mean age, 60.1 years; range, 46-73 years) from the Wisconsin Registry for Alzheimers Prevention. Using a qualitative rating, 18% of the samples were strongly positive Beta-amyloid (Aβ+), 41% indeterminate (Aβi), and 41% negative (Aβ-). Aβ+ was associated with older age, female sex, and showed trends for maternal family history of AD and APOE4. Relative to the Aβ- group, Aβ+ and Aβi participants had increased glucose metabolism in the bilateral thalamus; Aβ+ participants also had increased metabolism in the bilateral superior temporal gyrus. Aβ+ participants exhibited increased gray matter in the lateral parietal lobe bilaterally relative to the Aβ- group, and no areas of significant atrophy. Cognitive performance and self report cognitive and affective symptoms did not differ between groups. Amyloid burden can be identified in adults at a mean age of 60 years and is accompanied by glucometabolic increases in specific areas, but not atrophy or cognitive loss. This asymptomatic stage may be an opportune window for intervention to prevent progression to symptomatic AD.
Neuropsychology (journal) | 2010
N. Maritza Dowling; Bruce P. Hermann; Asenath La Rue; Mark A. Sager
OBJECTIVE To examine the latent structure of a test battery currently being used in a longitudinal study of asymptomatic middle-aged adults with a parental history of Alzheimers disease (AD) and test the invariance of the factor solution across subgroups defined by selected demographic variables and known genetic risk factors for AD. METHOD An exploratory factor analysis (EFA) and a sequence of confirmatory factor analyses (CFA) were conducted on 24 neuropsychological measures selected to provide a comprehensive estimate of cognitive abilities most likely to be affected in preclinical AD. Once the underlying latent model was defined and the structural validity established through model comparisons, a multigroup confirmatory factor analysis model was used to test for factorial invariance across groups. RESULTS The EFA solution revealed a factor structure consisting of five constructs: verbal ability, visuospatial ability, speed & executive function, working memory, and verbal learning & memory. The CFA models provided support for the hypothesized 5-factor structure. Results indicated factorial invariance of the model across all groups examined. CONCLUSIONS Collectively, the results suggested a relatively strong psychometric basis for using the factor structure in clinical samples that match the characteristics of this cohort. This confirmed an invariant factor structure should prove useful in research aimed to detect the earliest cognitive signature of preclinical AD in similar middle aged cohorts.
NeuroImage: Clinical | 2014
Annie M. Racine; Nagesh Adluru; Andrew L. Alexander; Bradley T. Christian; Ozioma C. Okonkwo; Jennifer M. Oh; Caitlin A. Cleary; Alex C. Birdsill; Ansel T. Hillmer; Dhanabalan Murali; Todd E. Barnhart; Catherine L. Gallagher; Cynthia M. Carlsson; Howard A. Rowley; N. Maritza Dowling; Sanjay Asthana; Mark A. Sager; Barbara B. Bendlin; Sterling C. Johnson
Some cognitively healthy individuals develop brain amyloid accumulation, suggestive of incipient Alzheimers disease (AD), but the effect of amyloid on other potentially informative imaging modalities, such as Diffusion Tensor Imaging (DTI), in characterizing brain changes in preclinical AD requires further exploration. In this study, a sample (N = 139, mean age 60.6, range 46 to 71) from the Wisconsin Registry for Alzheimers Prevention (WRAP), a cohort enriched for AD risk factors, was recruited for a multimodal imaging investigation that included DTI and [C-11]Pittsburgh Compound B (PiB) positron emission tomography (PET). Participants were grouped as amyloid positive (Aβ+), amyloid indeterminate (Aβi), or amyloid negative (Aβ−) based on the amount and pattern of amyloid deposition. Regional voxel-wise analyses of four DTI metrics, fractional anisotropy (FA), mean diffusivity (MD), axial diffusivity (Da), and radial diffusivity (Dr), were performed based on amyloid grouping. Three regions of interest (ROIs), the cingulum adjacent to the corpus callosum, hippocampal cingulum, and lateral fornix, were selected based on their involvement in the early stages of AD. Voxel-wise analysis revealed higher FA among Aβ+ compared to Aβ− in all three ROIs and in Aβi compared to Aβ− in the cingulum adjacent to the corpus callosum. Follow-up exploratory whole-brain analyses were consistent with the ROI findings, revealing multiple regions where higher FA was associated with greater amyloid. Lower fronto-lateral gray matter MD was associated with higher amyloid burden. Further investigation showed a negative correlation between MD and PiB signal, suggesting that Aβ accumulation impairs diffusion. Interestingly, these findings in a largely presymptomatic sample are in contradistinction to relationships reported in the literature in symptomatic disease stages of Mild Cognitive Impairment and AD, which usually show higher MD and lower FA. Together with analyses showing that cognitive function in these participants is not associated with any of the four DTI metrics, the present results suggest an early relationship between PiB and DTI, which may be a meaningful indicator of the initiating or compensatory mechanisms of AD prior to cognitive decline.
PLOS ONE | 2013
N. Maritza Dowling; Carey E. Gleason; JoAnn E. Manson; Howard N. Hodis; Virginia M. Miller; Eliot A. Brinton; Genevieve Neal-Perry; M. Nanette Santoro; Marcelle I. Cedars; Rogerio A. Lobo; Whitney Wharton; Frederick Naftolin; Hugh S. Taylor; S. Mitchell Harman; Sanjay Asthana
Objectives While global measures of cardiovascular (CV) risk are used to guide prevention and treatment decisions, these estimates fail to account for the considerable interindividual variability in pre-clinical risk status. This study investigated heterogeneity in CV risk factor profiles and its association with demographic, genetic, and cognitive variables. Methods A latent profile analysis was applied to data from 727 recently postmenopausal women enrolled in the Kronos Early Estrogen Prevention Study (KEEPS). Women were cognitively healthy, within three years of their last menstrual period, and free of current or past CV disease. Education level, apolipoprotein E ε4 allele (APOE4), ethnicity, and age were modeled as predictors of latent class membership. The association between class membership, characterizing CV risk profiles, and performance on five cognitive factors was examined. A supervised random forest algorithm with a 10-fold cross-validation estimator was used to test accuracy of CV risk classification. Results The best-fitting model generated two distinct phenotypic classes of CV risk 62% of women were “low-risk” and 38% “high-risk”. Women classified as low-risk outperformed high-risk women on language and mental flexibility tasks (p = 0.008) and a global measure of cognition (p = 0.029). Women with a college degree or above were more likely to be in the low-risk class (OR = 1.595, p = 0.044). Older age and a Hispanic ethnicity increased the probability of being at high-risk (OR = 1.140, p = 0.002; OR = 2.622, p = 0.012; respectively). The prevalence rate of APOE-ε4 was higher in the high-risk class compared with rates in the low-risk class. Conclusion Among recently menopausal women, significant heterogeneity in CV risk is associated with education level, age, ethnicity, and genetic indicators. The model-based latent classes were also associated with cognitive function. These differences may point to phenotypes for CV disease risk. Evaluating the evolution of phenotypes could in turn clarify preclinical disease, and screening and preventive strategies. ClinicalTrials.gov NCT00154180
Cerebral Cortex | 2014
Ozioma C. Okonkwo; Guofan Xu; Jennifer M. Oh; N. Maritza Dowling; Cynthia M. Carlsson; Catherine L. Gallagher; Alex C. Birdsill; Matthew Lee Palotti; Whitney Wharton; Bruce P. Hermann; Asenath LaRue; Barbara B. Bendlin; Howard A. Rowley; Sanjay Asthana; Mark A. Sager; Sterling C. Johnson
Cerebral blood flow (CBF) provides an indication of the metabolic status of the cortex and may have utility in elucidating preclinical brain changes in persons at risk for Alzheimers disease (AD) and related diseases. In this study, we investigated CBF in 327 well-characterized adults including patients with AD (n = 28), patients with amnestic mild cognitive impairment (aMCI, n = 23), older cognitively normal (OCN, n = 24) adults, and asymptomatic middle-aged adults (n = 252) with and without a family history (FH) of AD. Compared with the asymptomatic cohort, AD patients displayed significant hypoperfusion in the precuneus, posterior cingulate, lateral parietal cortex, and the hippocampal region. Patients with aMCI exhibited a similar but less marked pattern of hypoperfusion. Perfusion deficits within the OCN adults were primarily localized to the inferior parietal lobules. Asymptomatic participants with a maternal FH of AD showed hypoperfusion in hippocampal and parietofrontal regions compared with those without a FH of AD or those with only a paternal FH of AD. These observations persisted when gray matter volume was included as a voxel-wise covariate. Our findings suggest that having a mother with AD might confer a particular risk for AD-related cerebral hypoperfusion in midlife. In addition, they provide further support for the potential utility of arterial spin labeling for the measurement of AD-related neurometabolic dysfunction, particularly in situations where [18F]fluorodeoxyglucose imaging is infeasible or clinically contraindicated.
Alzheimer's & Dementia: Diagnosis, Assessment & Disease Monitoring | 2015
Stephanie A. Schultz; Jennifer M. Oh; Rebecca L. Koscik; N. Maritza Dowling; Catherine L. Gallagher; Cynthia M. Carlsson; Barbara B. Bendlin; Asenath LaRue; Bruce P. Hermann; Howard A. Rowley; Sanjay Asthana; Mark A. Sager; Sterling C. Johnson; Ozioma C. Okonkwo
Subjective memory complaints (SMCs) represent an individuals perception of subtle changes in memory in the absence of objective impairment in memory. However, it is not fully known whether persons with SMCs harbor brain alterations related to Alzheimers disease (AD) or whether they indeed demonstrate poorer cognitive performance.
Journal of The International Neuropsychological Society | 2011
N. Maritza Dowling; Sarah Tomaszewski Farias; Bruce Reed; Joshua A. Sonnen; Milton E. Strauss; Julie A. Schneider; David A. Bennett; Dan Mungas
Studies of neuropathology-cognition associations are not common and have been limited by small sample sizes, long intervals between autopsy and cognitive testing, and lack of breadth of neuropathology and cognition variables. This study examined domain-specific effects of common neuropathologies on cognition using data (N = 652) from two large cohort studies of older adults. We first identified dimensions of a battery of 17 neuropsychological tests, and regional measures of Alzheimers disease (AD) neuropathology. We then evaluated how cognitive factors were related to dimensions of AD and additional measures of cerebrovascular and Lewy Body disease, and also examined independent effects of brain weight. All cognitive domains had multiple neuropathology determinants that differed by domain. Neocortical neurofibrillary tangles were the strongest predictors of most domains, while medial temporal tangles showed a weaker relationship with episodic memory. Neuritic plaques had relatively strong effects on multiple domains. Lewy bodies and macroscopic infarcts were associated with all domains, while microscopic infarcts had more limited associations. Brain weight was related to all domains independent of specific neuropathologies. Results show that cognition is complexly determined by multiple disease substrates. Neuropathological variables and brain weight contributed approximately a third to half of the explained variance in different cognitive domains.