Smartwatches may be key to development of new Parkinson's treatments
Funding for the study was contributed by Biogen, Takeda, and the members of the Critical Path for Parkinson’s Consortium 3DT Initiative, Stage 2. Biogen and Takeda contributed to the following activities: design and conduct of the study; analysis and interpretation of the data; preparation, review, and approval of the manuscript; and decision to submit the manuscript for publication. The authors acknowledge Odinachi Oguh, MD for assistance in the conduct of the study.
Jamie L. Adams, Melissa A. Kostrzebski, Peggy Auinger, Peter Wilmot, Yvonne Pohlson, Emma Waddell, Stella Jensen-Roberts & E. Ray DorseyJamie L. Adams, Melissa A. Kostrzebski, Peggy Auinger & E. Ray DorseyTairmae Kangarloo, Brian Tracey, Patricio O’Donnell, Dmitri Volfson, Robert D.
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The cervical lymph node contributes to peripheral inflammation related to Parkinson’s disease - Journal of NeuroinflammationBackground Peripheral inflammation is an important feature of Parkinson’s disease (PD). However, if and how CNS pathology is involved in the peripheral inflammation in PD remains to be fully investigated. Recently, the existence of meningeal lymphatics and its involvement in draining cerebral spinal fluid (CSF) to the cervical lymph node has been discovered. It is known that meningeal lymphatic dysfunction exists in idiopathic PD. The deep cervical lymph node (dCLN) substantially contributes to the drainage of the meningeal lymphatics. In addition, one of the lymphatics draining components, CSF, contains abundant α-synuclein (α-syn), a protein critically involved in PD pathogenesis and neuroinflammation. Thus, we began with exploring the possible structural and functional alterations of the dCLN in a PD mouse model (A53T mice) and investigated the role of pathological α-syn in peripheral inflammation and its potential underlying molecular mechanisms. Methods In this study, the transgenic mice (prnp-SNCA*A53T) which specifically overexpressed A53T mutant α-syn in CNS were employed as the PD animal model. Immunofluorescent and Hematoxylin and eosin staining were used to evaluate structure of dCLN. Inflammation in dCLNs as well as in bone-marrow-derived macrophages (BMDMs) was assessed quantitatively by measuring the mRNA and protein levels of typical inflammatory cytokines (including IL-1β, IL-6 and TNF-α). Intra-cisterna magna injection, flow cytometric sorting and electrochemiluminescence immunoassays were applied to investigate the lymphatic drainage of α-syn from the CNS. RNA-seq and Western blot were used to explore how pathological α-syn mediated the inflammation in PD mice. Results The results unequivocally revealed substantially enlarged dCLNs, along with slow lymphatic flow, and increased inflammation in the dCLNs of A53T mice. Oligomeric α-syn drained from CSF potently activated macrophages in the dCLN via endoplasmic reticulum (ER) stress. Notably, inhibiti
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Visualizing reactive astrocyte-neuron interaction in Alzheimer’s disease using 11C-acetate and 18F-FDGNam et al. show that combining PET imaging with 11C-acetate and 18F-fluorodeoxyglucose tracers is a promising new approach for visualizing reactive astrogliosis
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