Evaluation of fMRI activation in post-stroke patients with movement disorders after repetitive transcranial magnetic stimulation: a scoping review

BackgroundMovement disorders are one of the most common stroke residual effects, which cause a major stress on their families and society. Repetitive transcranial magnetic stimulation (rTMS) could change neuroplasticity, which has been suggested as an alternative rehabilitative treatment for enhancing stroke recovery. Functional magnetic resonance imaging (fMRI) is a promising tool to explore neural mechanisms underlying rTMS intervention.ObjectOur primary goal is to better understand the neuroplastic mechanisms of rTMS in stroke rehabilitation, this paper provides a scoping review of recent studies, which investigate the alteration of brain activity using fMRI after the application of rTMS over the primary motor area (M1) in movement disorders patients after stroke.MethodThe database PubMed, Embase, Web of Science, WanFang Chinese database, ZhiWang Chinese database from establishment of each database until December 2022 were included. Two researchers reviewed the study, collected the information and the relevant characteristic extracted to a summary table. Two researchers also assessed the quality of literature with the Downs and Black criteria. When the two researchers unable to reach an agreement, a third researcher would have been consulted.ResultsSeven hundred and eleven studies in all were discovered in the databases, and nine were finally enrolled. They were of good quality or fair quality. The literature mainly involved the therapeutic effect and imaging mechanisms of rTMS on improving movement disorders after stroke. In all of them, there was improvement of the motor function post-rTMS treatment. Both high-frequency rTMS (HF-rTMS) and low-frequency rTMS (LF-rTMS) can induce increased functional connectivity, which may not directly correspond to the impact of rTMS on the activation of the stimulated brain areas. Comparing real rTMS with sham group, the neuroplastic effect of real rTMS can lead to better functional connectivity in the brain network in assisting stroke recovery.ConclusionrTMS allows the excitation and synchronization of neural activity, promotes the reorganization of brain function, and achieves the motor function recovery. fMRI can observe the influence of rTMS on brain networks and reveal the neuroplasticity mechanism of post-stroke rehabilitation. The scoping review helps us to put forward a series of recommendations that might guide future researchers exploring the effect of motor stroke treatments on brain connectivity

PET Imaging of Neuroinflammation in Alzheimer's Disease

Neuroinflammation play an important role in Alzheimer's disease pathogenesis. Advances in molecular imaging using positron emission tomography have provided insights into the time course of neuroinflammation and its relation with Alzheimer's disease central pathologies in patients and in animal disease models. Recent single-cell sequencing and transcriptomics indicate dynamic disease-associated microglia and astrocyte profiles in Alzheimer's disease. Mitochondrial 18-kDa translocator protein is the most widely investigated target for neuroinflammation imaging. New generation of translocator protein tracers with improved performance have been developed and evaluated along with tau and amyloid imaging for assessing the disease progression in Alzheimer's disease continuum. Given that translocator protein is not exclusively expressed in glia, alternative targets are under rapid development, such as monoamine oxidase B, matrix metalloproteinases, colony-stimulating factor 1 receptor, imidazoline-2 binding sites, cyclooxygenase, cannabinoid-2 receptor, purinergic P2X7 receptor, P2Y12 receptor, the fractalkine receptor, triggering receptor expressed on myeloid cells 2, and receptor for advanced glycation end products. Promising targets should demonstrate a higher specificity for cellular locations with exclusive expression in microglia or astrocyte and activation status (pro- or anti-inflammatory) with highly specific ligand to enable in vivo brain imaging. In this review, we summarised recent advances in the development of neuroinflammation imaging tracers and provided an outlook for promising targets in the future

ABIN1 (Q478) is Required to Prevent Hematopoietic Deficiencies through Regulating Type I IFNs Expression

Abstract A20‐binding inhibitor of NF‐κB activation (ABIN1) is a polyubiquitin‐binding protein that regulates cell death and immune responses. Although Abin1 is located on chromosome 5q in the region commonly deleted in patients with 5q minus syndrome, the most distinct of the myelodysplastic syndromes (MDSs), the precise role of ABIN1 in MDSs remains unknown. In this study, mice with a mutation disrupting the polyubiquitin‐binding site (Abin1Q478H/Q478H) is generated. These mice develop MDS‐like diseases characterized by anemia, thrombocytopenia, and megakaryocyte dysplasia. Extramedullary hematopoiesis and bone marrow failure are also observed in Abin1Q478H/Q478H mice. Although Abin1Q478H/Q478H cells are sensitive to RIPK1 kinase–RIPK3–MLKL‐dependent necroptosis, only anemia and splenomegaly are alleviated by RIPK3 deficiency but not by MLKL deficiency or the RIPK1 kinase‐dead mutation. This indicates that the necroptosis‐independent function of RIPK3 is critical for anemia development in Abin1Q478H/Q478H mice. Notably, Abin1Q478H/Q478H mice exhibit higher levels of type I interferon (IFN‐I) expression in bone marrow cells compared towild‐type mice. Consistently, blocking type I IFN signaling through the co‐deletion of Ifnar1 greatly ameliorated anemia, thrombocytopenia, and splenomegaly in Abin1Q478H/Q478H mice. Together, these results demonstrates that ABIN1(Q478) prevents the development of hematopoietic deficiencies by regulating type I IFN expression