Magnetization Dynamics of an Individual Single-Crystalline Fe-Filled Carbon Nanotube

The magnetization dynamics of individual Fe-filled multiwall carbon-nanotubes (FeCNT), grown by chemical vapor deposition, are investigated by microresonator ferromagnetic resonance (FMR) and Brillouin light scattering (BLS) microscopy and corroborated by micromagnetic simulations. Currently, only static magnetometry measurements are available. They suggest that the FeCNTs consist of a single-crystalline Fe nanowire throughout the length. The number and structure of the FMR lines and the abrupt decay of the spin-wave transport seen in BLS indicate, however, that the Fe filling is not a single straight piece along the length. Therefore, a stepwise cutting procedure is applied in order to investigate the evolution of the ferromagnetic resonance lines as a function of the nanowire length. The results show that the FeCNT is indeed not homogeneous along the full length but is built from 300 to 400 nm long single-crystalline segments. These segments consist of magnetically high quality Fe nanowires with almost the bulk values of Fe and with a similar small damping in relation to thin films, promoting FeCNTs as appealing candidates for spin-wave transport in magnonic applications. © 2019 The Authors. Published by WILEY-VCH Verlag GmbH & Co. KGaA, Weinhei

FDG-PET underscores the key role of the thalamus in frontotemporal lobar degeneration caused by C9ORF72 mutations

C9ORF72 mutations are the most common cause of familial frontotemporal lobar degeneration (FTLD) and amyotrophic lateral sclerosis (ALS). MRI studies have investigated structural changes in C9ORF72-associated FTLD (C9FTLD) and provided first insights about a prominent involvement of the thalamus and the cerebellum. Our multicenter, F-18-fluorodeoxyglucose positron-emission tomography study of 22 mutation carriers with FTLD, 22 matched non-carriers with FTLD, and 23 cognitively healthy controls provided valuable insights into functional changes in C9FTLD: compared to non-carriers, mutation carriers showed a significant reduction of glucose metabolism in both thalami, underscoring the key role of the thalamus in C9FTLD. Thalamic metabolism did not correlate with disease severity, duration of disease, or the presence of psychotic symptoms. Against our expectations we could not demonstrate a cerebellar hypometabolism in carriers or non-carriers. Future imaging and neuropathological studies in large patient cohorts are required to further elucidate the central role of the thalamus in C9FTLD

Clinico-genetic findings in 509 frontotemporal dementia patients

Abstract Frontotemporal dementia (FTD) is a clinically and genetically heterogeneous disorder. To which extent genetic aberrations dictate clinical presentation remains elusive. We investigated the spectrum of genetic causes and assessed the genotype-driven differences in biomarker profiles, disease severity and clinical manifestation by recruiting 509 FTD patients from different centers of the German FTLD consortium where individuals were clinically assessed including biomarker analysis. Exome sequencing as well as C9orf72 repeat analysis were performed in all patients. These genetic analyses resulted in a diagnostic yield of 18.1%. Pathogenic variants in C9orf72 (n = 47), GRN (n = 26), MAPT (n = 11), TBK1 (n = 5), FUS (n = 1), TARDBP (n = 1), and CTSF (n = 1) were identified across all clinical subtypes of FTD. TBK1-associated FTD was frequent accounting for 5.4% of solved cases. Detection of a homozygous missense variant verified CTSF as an FTD gene. ABCA7 was identified as a candidate gene for monogenic FTD. The distribution of APOE alleles did not differ significantly between FTD patients and the average population. Male sex was weakly associated with clinical manifestation of the behavioral variant of FTD. Age of onset was lowest in MAPT patients. Further, high CSF neurofilament light chain levels were found to be related to GRN-associated FTD. Our study provides large-scale retrospective clinico-genetic data such as on disease manifestation and progression of FTD. These data will be relevant for counseling patients and their families

Postablation asymptomatic cerebral lesions: Long-term follow-up using magnetic resonance imaging

BACKGROUND Catheter ablation of atrial fibrillation (AF) is complicated by cerebral emboli resulting in acute ischemia. Recently, cerebral ischemic microlesions have been identified with diffusion-weighted magnet resonance imaging (MRI). OBJECTIVE The clinical course and longer-term characteristics of these lesions are not known and were investigated in this study. METHODS Of 86 patients, 33 (38%) had new asymptomatic cerebral lesions documented on MRI after catheter ablation for AF; 14 of these 33 (42%) underwent repeat MRI at different time intervals (2 weeks to 1 year) during follow-up, and clinical symptoms as well as size and number of residual lesions were documented. RESULTS In postablation cerebral MRI, 50 new lesions were identified (3.6 lesions/patient) in 14 patients. No patient presented any neurological symptoms. Distribution of the lesions was predominantly in the left hemisphere (60%) and the cerebellum (26%); 52% of the lesions were small (10 mm. Follow-up MRI after a median of 3 months revealed 3 residual lesions in 3 of 14 patients corresponding to the large acute postablation lesions (>10 mm). The re-maining 47 of 50 (94%) of the small or medium-sized lesions were not detectable at follow-up evaluation. CONCLUSIONS Most asymptomatic cerebral lesions observed acutely after AF ablation procedures were 2 weeks after ablation. The larger acute lesions produced chronic glial scars. Neither chronic nor acute lesions were associated with neurological symptoms