Objectives: Amyloid-lowering immunotherapies can cause amyloid-related imaging abnormalities (ARIA), requiring brain MRI for detection and monitoring. The European Society of Neuroradiology (ESNR)/European Academy of Neurology (EAN) ARIA Working Group conducted a survey to assess European clinicians’ readiness for this logistical challenge and need for further education on ARIA. Materials and methods: An online questionnaire with 32 items (multiple choice, single best choice, and free text) was distributed to ESNR and EAN members. Between June and July 2024, we collected 422 responses from 41 European countries, including 47% neurologists and 51% (neuro)radiologists; 15% were residents, and 58% worked in academic hospitals. Results: Of respondents, 69% were familiar with the concept of ARIA, and 60% reportedly understood its risk factors. Confidence in evaluating ARIA-E (edema/effusion) and ARIA-H (hemorrhage) subtypes was reported by 60% and 69%, respectively, with (neuro)radiologists more confident than neurologists. However, 34% of respondents felt poorly equipped to meet logistical demands, and 82% lacked a dedicated ARIA imaging protocol. Key barriers included limited organizational adaptability and radiology expertise. Notably, 72% saw potential in having support by artificial intelligence approaches, and 93% expressed the wish for further training on how to monitor ARIA. Conclusions: Despite the current unavailability of amyloid-lowering therapies, European neurologists and (neuro)radiologists report reasonable ARIA awareness. There is a clear need for additional practical preparation and training in ARIA assessment, which can inform future ESNR/EAN educational initiatives. Key Points: Question Are neurologists and neuroradiologists ready for ARIA monitoring? Findings Neurologists and neuroradiologists were moderately familiar with the concept of ARIA, its risk factors, and its identification on MRI, but felt poorly equipped to meet the logistical demands. Clinical relevance With the potential introduction of amyloid-lowering therapies in European countries, identifying key barriers, such as limited organizational adaptability and radiology expertise, highlights the need for further practical preparation by clinical departments and additional training in ARIA assessment.

BACKGROUND: White matter hyperintensities (WMHs) of presumed vascular origin are common in the elderly and are associated with vascular risk factors. There is evidence that vascular risk factors, in particular hypertension, are associated with WMH in particular locations of the white matter. However, it remains unclear whether this is true for all risk factors and whether signature WMH locations differ between risk factors. We aimed to identify WMH locations associated with vascular risk factors in community-dwelling individuals. METHODS: We pooled cross-sectional data from 16 population-based cohorts (15 653 individuals; mean age, 64.2±11.8 years; 52.2% female) through the Meta VCI Map Consortium. We quantified associations between WMH volumes in 50 white matter regions and 6 vascular risk factors using linear mixed models. Analyses were corrected for age, sex, study site, and total WMH volume. RESULTS: Hypertension (B=0.141; P<0.001), smoking (B=0.096; P<0.001), diabetes (B=0.059; P<0.001), and history of vascular disease (B=0.056; P=0.034) were significantly associated with higher total WMH volume, whereas obesity (B=0.023; P=0.139) and hypercholesterolemia (B=0.009; P=0.531) were not. After correcting for total WMH volume, hypertension was associated with WMH volume in 10 regions (ie, bilateral external capsule, superior longitudinal fasciculus, superior corona radiata, anterior limb of the internal capsule, left anterior corona radiata, and left superior fronto-occipital fasciculus), smoking (body corpus callosum), diabetes (genu corpus callosum), and obesity (left inferior fronto-occipital fasciculus), each with one region. CONCLUSIONS: Hypertension has a signature WMH pattern, whereas associations between other vascular risk factors and regional WMH volumes seem to be mainly explained by a global increase in WMH rather than region-specific effects.

Objective: Women with anorexia nervosa (AN) have been shown to demonstrate differences in functional connectivity in brain regions associated with cognitive control, somatosensory processing, and emotion regulation. However, previous studies have been conducted on small samples and have inconsistent findings. Therefore, this study aimed to identify aberrant brain networks related to the core clinical symptoms of AN and to explore the longitudinal association with clinical outcome in a large population of adolescents experiencing their first episode of AN. Methods: Functional MRI (fMRI) of brain resting-state functional connectivity (RS-FC) of female adolescents with first-onset AN (n = 56) were compared to age- and education-matched typically developing (TD) adolescents (n = 64). To account for the severity of underweight, separate analyses were performed to investigate differences in RS-FC between underweight AN participants and TD adolescents, as well as between underweight (n = 30) and weight-restored AN (n = 26) participants. Clinical outcomes, i.e. body mass index and eating disorder (ED) symptoms, were assessed at baseline and one-year follow-up. Independent component analyses (ICA) were used to extract the brain networks of interest: the default mode (DMN), left and right frontoparietal (FPN), and the insular (IN) networks. Linear regression analyses were conducted to assess differences in RS-FC between AN and TD participants, as well as to assess whether RS-FC was associated with clinical symptoms at baseline and at one-year of follow-up. Two statistical models were used: model 1 adjusted for age and socioeconomic status (SES), and model 2 additionally adjusted for baseline anxiety and depressive symptoms. Results: Underweight AN participants had lower RS-FC between the DMN-IN, as well as between the FPN-IN compared to the TD adolescents. After correction for multiple testing, no significant differences in RS-FC were found between underweight AN participants and weight-restored AN participants, as well as between the whole AN group and the TD group. RS-FC was not associated with the severity of clinical symptoms at baseline nor at one-year of follow-up. Conclusion: AN is associated with changes in RS-FC between the FPN-IN and DMN-IN during the underweight state. These changes in RS-FC were no longer observed in weight-restored AN participants, emphasizing the impact of underweight on RS-FC in AN. Changes in these brain networks may partly explain the impaired cognitive control and difficulties with emotion and behavioral regulation in individuals with AN during the underweight state.

Objective To identify common genetic variants associated with the presence of brain microbleeds (BMBs).MethodsWe performed genome-wide association studies in 11 population-based cohort studies and 3 case-control or case-only stroke cohorts. Genotypes were imputed to the Haplotype Reference Consortium or 1000 Genomes reference panel. BMBs were rated on susceptibility-weighted or T2*-weighted gradient echo MRI sequences, and further classified as lobar or mixed (including strictly deep and infratentorial, possibly with lobar BMB). In a subset, we assessed the effects of APOE ϵ2 and ϵ4 alleles on BMB counts. We also related previously identified cerebral small vessel disease variants to BMBs.ResultsBMBs were detected in 3,556 of the 25,862 participants, of which 2,179 were strictly lobar and 1,293 mixed. One locus in the APOE region reached genome-wide significance for its association with BMB (lead single nucleotide polymorphism rs769449; odds ratio [OR]any BMB [95% confidence interval (CI)] 1.33 [1.21-1.45]; p = 2.5 × 10-10). APOE ϵ4 alleles were associated with strictly lobar (OR [95% CI] 1.34 [1.19-1.50]; p = 1.0 × 10-6) but not with mixed BMB counts (OR [95% CI] 1.04 [0.86-1.25]; p = 0.68). APOE ϵ2 alleles did not show associations with BMB counts. Variants previously related to deep intracerebral hemorrhage and lacunar stroke, and a risk score of cerebral white matter hyperintensity variants, were associated with BMB.ConclusionsGenetic variants in the APOE region are associated with the presence of BMB, most likely due to the APOE ϵ4 allele count related to a higher number of strictly lobar BMBs. Genetic predisposition to small vessel disease confers risk of BMB, indicating genetic overlap with other cerebral small vessel disease markers.