Coefficient of variation for repeated measurements of phantom ADC along each of the main orthogonal directions ( - <i>i</i> = 1, readout/left-right; <i>i</i> = 2, phase-encoding/anterior-posterior; <i>i</i> = 3, slice-selection/head-foot) for scanner-A, scanner-B and scanner-C.

<p>The bar charts depict the mean value ± standard deviation within ROI_ref.</p

Phantom ADC along each of the main orthogonal directions (ADC_i - <i>i</i> = 1, readout/left-right; <i>i</i> = 2, phase-encoding/anterior-posterior; <i>i</i> = 3, slice-selection/head-foot) for scanner-A, scanner-B and scanner-C.

<p>The bar charts depict the mean of the average value within ROI_ref ± standard deviation across five repetitions. The dashed line represents the known phantom diffusion coefficient (2.14±0.03×10⁻³ mm²/s) at the reference temperature value of 22°C.</p

Non-uniformity of maps of phantom ADC along each of the main orthogonal directions ( - <i>i</i> = 1, readout/left-right; <i>i</i> = 2, phase-encoding/anterior-posterior; <i>i</i> = 3, slice-selection/head-foot) for scanner-A, scanner-B and scanner-C.

<p>The bar charts depict the mean value ± standard deviation across five repetitions.</p

Is neuroticism differentially associated with risk of Alzheimer’s disease, vascular dementia, and frontotemporal dementia?

This study examines whether neuroticism is differentially associated with risk of incident Alzheimer's disease (AD), vascular dementia (VD), and frontotemporal dementia (FTD) using a prospective study design. Participants from the UK Biobank (N = 401,422) completed a self-report neuroticism scale in 2006–2010 and incident all-cause dementia, AD, VD, and FTD were ascertained using electronic health records or death records up to 2018. During an average follow-up of 8.8 years (3,566,123 person-years), there were 1798 incident of all-cause dementia, 675 AD, 376 VD, and 81 FTD. Accounting for age and sex, compared to individuals in the low quartile, individuals in the top quartile of neuroticism had higher risk of all-cause dementia (HR = 1.70; 95% CI: 1.49–1.93), AD (HR = 1.42; 1.15–1.75), VD (HR = 1.73; 1.30–2.29), but not FTD (HR = 0.89; 0.49–1.63). The associations with AD and VD were attenuated but remained significant after further accounting for education, household income, deprivation index, diabetes, hypertension, stroke, heart attack, ever smoker, physical activity, obesity, hemoglobin A1c, C-reactive protein, and low-density lipoprotein. The associations were not moderated by socioeconomic status. The findings were consistent in analyses that excluded cases that occurred within the first 5 years of follow-up. In conclusion, neuroticism is a robust predictor of incident AD and VD, but not FTD. This pattern suggests that the affective symptoms that distinguish dementia types may partly reflect premorbid differences in trait neuroticism.</p

Left: velocity curves for eyelid-jaw synkinesis in a patient with familial Marcus Gunn jaw-winking synkinesis (MGJWS).

<p>Black line represents velocity trace of jaw movement, gray line represents velocity trace of eyelid movement. The x-axis corresponds to time (ms) and the y-axis to velocity (mm/s). The first peak in the velocity trace corresponds to the peak velocity of the opening phase, the second peak-to-peak velocity of the closing phase. Right: Upper panel. Correlation between jaw opening duration and eyelid opening duration expressed in milliseconds. Lower panel. Correlation between jaw closing duration and eyelid closing duration expressed in milliseconds.</p

Significant reduction in FA (voxels in red) in the brainstem of a patient with familial Marcus Gunn jaw-winking synkinesis (MGJWS) overlaid on the MNI T1 non-linear template image.

<p>The FA alterations are localized within the midbrain tegmentum, the reticular formation and the central tegmental tracts.</p

Demographic, genetic and clinical data in 10 SCA2 patients.

<p>F, female; IACRS, Inherited Ataxia Clinical Rating Scale; M, male; SD, standard deviation.</p

Results of the baseline between group (SCA2 vs. controls) TBM analysis.

<p>Voxel-wise corrected p-value maps (threshold-free cluster enhancement, TFCE), testing the null hypothesis of zero differences in <b>|J|</b>_baseline between SCA2 patients and healthy controls. Highlighted clusters indicate significantly (p<0.05) more pronounced mean atrophy in SCA2 patients when compared to healthy controls (i.e. <b>|J|</b>_baseline in SCA2 patients significantly lower than <b>|J|</b>_baseline in healthy controls). All maps are overlayed on population-specific T1 template. These maps show significant symmetric atrophic changes in SCA2 patients (with respect to controls) in the brainstem, middle cerebellar peduncels, and cerebellar WM and adjacent cortical GM. No significant differences are observed in the supratentorial compartment.</p