Objective: To investigate the association between periventricular white mater hyperintensities (PVWMH) and biomarkers of elevated cerebral b-amyloid (Ab) in the Alzheimer's Disease Neuroimaging Initiative, a large prospective multicenter observational study. Methods:The burden of frontal, parietal, and occipital PVWMH on 3T fluid-attenuated inversion recovery MRI was evaluated in 698 cognitively normal participants and participants with mild cognitive impairment (MCI) using a novel semiquantitative visual rating scale. Results were correlated with CSF-Ab, florbetapir-PET, and fluorodeoxyglucose (FDG)-PET.Results: Increased burden of parietal, occipital, and frontal PVWMH was associated with elevated cerebral amyloid evidenced by high florbetapir-PET signal (p , 0.01) and low CSF-Ab (p , 0.01).In logistic regression models, including PVWMH, age, sex, APOE status, vascular risk factors, pulse pressure, vascular secondary prevention medications, education, ethnicity, and race, parietal, occipital, and frontal PVWMH burden was independently associated with high florbetapir-PET uptake (p , 0.05). In a similar logistic regression model, parietal and occipital (p , 0.05) but not frontal (p 5 0.05) PVWMH were independently associated with CSF-Ab. Weaker associations were found between parieto-occipital PVWMH and elevated CSF-tau (p , 0.05) and occipital PVWMH and elevated CSF-phospho-tau (p , 0.05). PVWMH were associated with cerebral hypometabolism on FDG-PET independent of CSF-Ab levels (p , 0.05). Absolute and consistency of agreement intraclass correlation coefficients were, respectively, 0.83 and 0.83 for frontal, 0.78 and 0.8 for parietal, and 0.45 and 0.75 for occipital PVWMH measurements.Conclusions: Increased PVWMH were associated with elevated cerebral amyloid independent of potential confounders such as age, APOE genotype, and vascular risk factors. The mechanisms underlying the association between PVWMH and cerebral amyloid remain to be clarified. Pathologic and imaging studies have shown that in Alzheimer disease (AD), cerebral small vessel disease (SVD) is coexistent in up to 80% and hastens cognitive deterioration.1 Whether this reflects parallel neuronal injury or synergistic worsening of AD pathogenic mechanisms remains unclear. 2There has been recent interest in the putative role of SVD in disruption of physiologic interstitial fluid bulk flow and paravascular mechanisms of b-amyloid (Ab) clearance.3 If SVD is an

Background: Skeletal infection with Acinetobacter baumannii is a rare condition and found mainly among soldiers injured in war. Multidrug resistant (MDR)

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2) longitudinally with abnormal hippocampal atrophy rates (NEU/ L+). Cut-off points were derived optimizing sensitivity and specificity in discriminating AMY-controls from AMY+ AD patients. Results: Forty-one patients were designated as SNAP using crosssectional and 22 using longitudinal measures (overlap¼12). No patient converted to dementia after 24 months. In addition, 123 were classified as AMY+NEU/C+ and 86 AMY+NEU/L+ (overlap¼63) with the first group showing a higher conversion rate (41 vs 31%). The highest conversion rate was observed for those positive on both neurodegeneration measures (49%). The opposite pattern was observed in the 77 patients designated as AMY+NEU/C-and 114 as AMY+NEU/L-(overlap¼54), with the first group showing a lower conversion rate (16 vs 23%). Thus, when using a crosssectional measure for neurodegeneration, 78% of the converters were placed in the AMY+NEU+ group compared to 59% with a longitudinal measure. Sixty-nine were AMY-NEU/C-and 88 AMY-NEU/L-(overlap¼59). No difference in conversion was observed (1.4-1.7%). Conclusions: Considerable differences in prevalence were observed when defining NEU+ and NEU-groups based on cross-sectional versus longitudinal data. For the SNAP groups no difference was observed in conversion to dementia, and in this respect it is unclear which measure is more appropriate to define SNAP. Perhaps both measures capture neurodegenerative change, but reflect different rates of injury to the hippocampus. Interestingly, for the AMY+NEU+ group a cross-sectional neurodegeneration measure was more closely linked to conversion to dementia than a longitudinal one.