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Alzheimer's disease and related dementias (ADRD) is two times more prevalent among compared to non-Hispanic Whites. Despite the higher prevalence of ADRD among older African Americans, recent estimates suggest research enrollment by those who identify as African American remains limited. The purpose of the study is to 1) explore how a culturally tailored community education program impacts clinical trial interest and enrollment in ADRD research studies and to 2) identify how applicable the African American community perceived the culturally tailored curriculum. Using a community-engaged research approach, we collaborated with predominately African American serving community-based organizations to support content development and delivery of Aging with Grace (AWG), a culturally tailored ADRD educational curriculum. A total of five AWG presentations were given to 66 attendees. Most attendees (67%) expressed interest in participating in clinical trials after attending AWG. Enrollment increased within an observational study (84%) and lifestyle prevention clinical trials (52%) from 2018 to 2019. Attendees (32%) also perceived an increase in ADRD knowledge from attending AWG and 89.1% believed more African Americans should participate in research. Our work demonstrates the effectiveness of a culturally tailored community education program to enhance knowledge, clinical trial interest, and recruitment into observational studies and lifestyle ADRD clinical trials among older African Americans. Education programs developed in partnership with the community can serve as bridge to research participation for underrepresented minorities in clinical research. Future studies should assess long-term retention of knowledge and research readiness.

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Despite older racial and ethnic minorities (REMs) being more likely to develop dementia they are underrepresented in clinical trials focused on neurological disorders. Inclusion of REMs in dementia prevention studies is vital to reducing the impact of disparities in dementia risk. We conducted a systematic review to characterize the number of REM enrolled in brain health and prevention randomized controlled trials (RCTs). RTCs published from January 1, 2004 to April 21, 2020 were included. Participants were normal cognitive adults aged 45 years and older who participated in a Phase II or Phase III U.S. based preventative trial. Analyses were performed to examine differences in trial characteristics between RCTs that did and those that did not report race/ethnicity and to calculate the pooled proportion of each racial/ethnic group in randomized brain healthy prevention trials. A total of 42 studies consisting of 100,748 participants were included in the final analyses. A total of 26 (62%) reported some racial/ethnic identity data. The pooled proportion of REM participants was 0.256 (95% CI, 0.191, 0.326). There is a lack of racial/ethnic reporting of participants and REMs remain underrepresented in brain health prevention RCTs.

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We encountered a problem in which a study's experimental design called for the use of paired data, but the pairing between subjects had been lost during the data collection procedure. Thus we were presented with a data set consisting of pre and post responses but with no way of determining the dependencies between our observed pre and post values. The aim of the study was to assess whether an intervention called Self-Revelatory Performance had an impact on participant's perceptions of Alzheimer's disease. The participant's responses were measured on an Affect grid before the intervention and on a separate grid after. To address the underlying question in light of the lost pairing we utilized a modified bootstrap approach to create a null hypothesized distribution for our test statistic, which was the distance between the two Affect Grids' Centers of Mass. Using this approach we were able to reject our null hypothesis and conclude that there was evidence the intervention influenced perceptions about the disease.

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The objective of this study was to investigate the relationship between cardiorespiratory (CR) fitness and the brain's white matter tract integrity using diffusion tensor imaging (DTI) in the Alzheimer's disease (AD) population. We recruited older adults in the early stages of AD (n = 37; CDR = 0.5 and 1) and collected cross-sectional fitness and diffusion imaging data. We examined the association between CR fitness (peak oxygen consumption [VO2peak]) and fractional anisotropy (FA) in AD-related white matter tracts using two processing methodologies: a tract-of-interest approach and tract-based spatial statistic (TBSS). Subsequent diffusivity metrics (radial diffusivity [RD], mean diffusivity [MD], and axial diffusivity [A × D]) were also correlated with VO2peak. The tract-of-interest approach showed that higher VO2peak was associated with preserved white matter integrity as measured by increased FA in the right inferior fronto-occipital fasciculus (p = 0.035, r = 0.36). We did not find a significant correlation using TBSS, though there was a trend for a positive association between white matter integrity and higher VO2peak measures (p < 0.01 uncorrected). Our findings indicate that higher CR fitness levels in early AD participants may be related to preserved white matter integrity. However to draw stronger conclusions, further study on the relationship between fitness and white matter deterioration in AD is necessary.

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The goal of this study was to compare insulin resistance in aging and aging-related neurodegenerative diseases, and to determine the relationship between insulin resistance and gray matter volume (GMV) in each cohort using an unbiased, voxel-based approach. Insulin resistance was estimated in apparently healthy elderly control (HC, n=21) and neurodegenerative disease (Alzheimer's disease (AD), n=20; Parkinson's disease (PD), n=22) groups using Homeostasis Model Assessment of Insulin Resistance 2 (HOMA2) and intravenous glucose tolerance test (IVGTT). HOMA2 and GMV were assessed within groups through General Linear Model multiple regression. We found that HOMA2 was increased in both AD and PD compared to the HC group (HC vs. AD, p=0.002, HC vs. PD, p=0.003), although only AD subjects exhibited increased fasting glucose (p=0.005). Furthermore, our voxel-based morphometry analysis revealed that HOMA2 was related to GMV in all cohorts in a region-specific manner (p<0.001, uncorrected). Significant relationships were observed in the medial prefrontal cortex (HC), medial temporal regions (AD), and parietal regions (PD). Finally, the directionality of the relationship between HOMA2 and GMV was disease-specific. Both HC and AD subjects exhibited negative relationships between HOMA2 and brain volume (increased HOMA2 associated with decreased brain volume), while a positive relationship was observed in PD. This cross-sectional study suggests that insulin resistance is increased in neurodegenerative disease, and that individuals with AD appear to have more severe metabolic dysfunction than individuals with PD or PD dementia.

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OBJECTIVE: Both low and high body mass index (BMI) has been associated with cognitive impairment and dementia risk, including Alzheimer disease (AD). We examined the relationship of BMI with potential underlying biological substrates for cognitive impairment. METHODS: We analyzed cross-sectional data from participants enrolled in the Alzheimer's Disease Neuroimaging Initiative (ADNI) with PET imaging using Pittsburgh Compound B (PiB, n = 101) or CSF analyses (n = 405) for ß-amyloid peptide (Aß) and total tau. We assessed the relationship of CSF biomarkers and global PiB uptake with BMI using linear regression controlling for age and sex. We also assessed BMI differences between those who were and were not considered biomarker positive. Finally, we assessed BMI change over 2 years in relationship to AD biomarkers. RESULTS: No dementia, mild cognitive impairment (MCI), and AD groups were not different in age, education, or BMI. In the overall sample, CSF Aß (ß = 0.181, p < 0.001), tau (ß = -0.179, p < 0.001), tau/Aß ratio (ß = -0.180, p < 0.001), and global PiB uptake (ß = -0.272, p = 0.005) were associated with BMI, with markers of increased AD burden associated with lower BMI. Fewer overweight individuals had biomarker levels indicative of pathophysiology (p < 0.01). These relationships were strongest in the MCI and no dementia groups. CONCLUSIONS: The presence and burden of in vivo biomarkers of cerebral amyloid and tau are associated with lower BMI in cognitively normal and MCI individuals. This supports previous findings of systemic change in the earliest phases of the disease. Further, MCI in those who are overweight may be more likely to result from heterogeneous pathophysiology.

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Somatosensation is thought to play an important role in skilled motor learning. The present study investigated how healthy adults learn a continuous implicit motor task when somatosensation is altered by 1 Hz repetitive transcranial magnetic stimulation (rTMS) delivered over the primary somatosensory cortex (S1). Twenty-seven right-handed participants enrolled in a two-part experiment. In Experiment 1, we verified that 20 min of 1 Hz rTMS over S1 disrupted cutaneous somatosensation (indexed by two-point discrimination) in the wrist/hand; the impact of 1 Hz rTMS on wrist proprioception (tested by limb-position matching) was variable. Sham rTMS had no effect on either measure. We exploited these effects in Experiment 2 by pairing either 1 Hz or sham rTMS with practice of a continuous tracking task over two separate sessions on different days. Implicit motor learning was indexed on a third, separate retention test day when no rTMS was delivered. Across practice in Experiment 2, both the 1 Hz and sham rTMS groups showed improved tracking performance; however, 1 Hz rTMS was associated with less accurate tracking and smaller improvements in performance. Importantly, at the no rTMS retention test the effects of altering sensation with stimulation over S1 were still evident in the persistently less accurate tracking behavior of the 1 Hz rTMS group. The current study shows that disruption of somatosensation during task practice impairs the magnitude of change associated with motor learning, perhaps through the development of an inaccurate internal model.

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OBJECTIVE: A consistently identified risk factor for Alzheimer disease (AD) is family history of dementia, with maternal transmission significantly more frequent than paternal transmission. A history of maternal AD may be related to AD-like glucose consumption in cognitively healthy subjects. In this cross-sectional study, we tested whether cognitively healthy people with a family history of AD have less gray matter volume (GMV), an endophenotype for late-onset AD, than individuals with no family history, and whether decreases in GMV are different in subjects with a maternal family history. METHODS: As part of the Kansas University Brain Aging Project, 67 cognitively intact individuals with a maternal history of late-onset AD (FHm, n = 16), a paternal history of AD (FHp, n = 8), or no parental history of AD (FH-, n = 43), similar in age, gender, education, and Mini-Mental State Examination score, were scanned at 3 T. We used voxel-based morphometry to examine GMV differences between groups, controlling for age, gender, and apoE4. RESULTS: Cognitively healthy individuals with a family history of late-onset AD had significantly decreased GMV in the precuneus, middle frontal, inferior frontal, and superior frontal gyri compared with FH- individuals. FHm subjects had significantly smaller inferior frontal, middle frontal, precuneus, and lingual gyri compared with FH- and FHp subjects. CONCLUSIONS: Overall, maternal family history of Alzheimer disease (AD) in cognitively normal individuals is associated with lower gray matter volume in AD-vulnerable brain regions. These data complement and extend reports of cerebral metabolic differences in subjects with a maternal family history.

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Our main aim was to determine whether individuals with stroke that affected the basal ganglia, organized movement sequences into chunks in the same fashion as neurologically intact individuals. To address this question, we compared motor response times during the performance of repeated sequences that were learned, and thus may be planned in advance, with random sequences where there is minimal if any advance preparation or organization of responses. The pattern of responses illustrated that, after basal ganglia stroke, individuals do not chunk elements of the repeated sequence into functional sub-sequences of movement to the same extent as neurologically intact age-matched people. Limited chunking of learned movements after stroke may explain past findings that show overall slower responses even when sequences of action are learned by this population. Further, our data in combination with other work, suggest that chunking may be a function of the basal ganglia.

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Fitts' law predicts that there is an essential trade-off between speed and accuracy during movement. Past investigations of Fitts' law have not characterized whether advance planning of upcoming fast and accurate movements impacts either behavior or patterns of brain activation. With an event-related functional magnetic resonance imaging (fMRI) paradigm, we investigated the neural correlates of advance planning and movement difficulty of rapid, goal-directed aimed movements using a discrete version of the classic Fitts' task. Our behavioral data revealed strong differences in response time, initial movement velocity, and end-point accuracy based on manipulation of both time to plan movements and response difficulty. We discovered a modulation of the neural network associated with executing the Fitts' task that was dependent on the availability of time to plan the upcoming movement and motor difficulty. Specifically, when time to plan for the upcoming movement was available, medial frontal gyrus (BA 10), pre-SMA (BA 6), putamen and cerebellar lobule VI were uniquely active to plan movements. Further, their activation correlated with behavioral measures of movement. In contrast, manipulating movement difficulty invoked a different pattern of brain activations in regions that are known to participate in motor control, including supplementary motor area (BA 6), sensory motor cortex (BA 4, 3, 2) and putamen. Our finding that medial frontal gyrus (BA 10) was important for discrete, fast and accurate movements expands the known role of this brain region, which in the past has been identified as a cognitive processing system supporting stimulus-oriented attending. We now extend this conceptualization to include motor functions such as those employed for processing for rapid, goal-directed aimed movements.

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The focus of this study was to determine whether minimal levels of exercise could halt the formation of diabetes-induced heart pathology. Seven-week-old male rats were divided into four groups: sedentary nondiabetic, exercise-trained non-diabetic, sedentary diabetic and exercise-trained diabetic. Individualised exercise programmes were based on the animal's tolerance, and continued for 7 weeks after the induction of diabetes. At the completion of the study, no differences were found in skeletal muscle citrate synthase activity between diabetic sedentary and exercise-trained rats, indicating that the exercise was low intensity. Diabetes-induced heart hypertrophy was not reversed with exercise as measured by heart-to-body weight ratios and EKG (R wave height). There was no statistical difference between groups in the response to an exercise stress test prior to the induction of diabetes. However, 4 weeks of diabetes resulted in a significant decrease in resting and post-stress test heart rates (9% and 20%, respectively), which remained depressed at week 7. The sedentary diabetic animals demonstrated an abnormal response during the recovery period of the EKG exercise test, which was not present in non-diabetic or exercise-trained diabetic animals. In conclusion, lowintensity exercise training improved the cardiac response to an exercise stress test in diabetic animals.

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