PMID-sentid Pub_year Sent_text comp_official_name comp_offsetprotein_name organism prot_offset 35327661-3 2022 The abundance of nAbs against alphaSyn is altered in patients with PD. nabs 17-21 synuclein alpha Homo sapiens 30-38 35327661-4 2022 In this work, we biophysically characterized nAbs against alphaSyn (nAbs-alphaSyn) and determined their biological effects. nabs 68-72 synuclein alpha Homo sapiens 58-66 35327661-8 2022 Specific binding of nAbs-alphaSyn to monomeric alphaSyn was demonstrated by Dot blot, ELISA, and Surface Plasmon Resonance. nabs 20-24 synuclein alpha Homo sapiens 47-55 35327661-13 2022 The results demonstrate that serum of healthy individuals contains nAbs that specifically bind alphaSyn and inhibit aggregation of alphaSyn in vitro. nabs 67-71 synuclein alpha Homo sapiens 95-103 35327661-13 2022 The results demonstrate that serum of healthy individuals contains nAbs that specifically bind alphaSyn and inhibit aggregation of alphaSyn in vitro. nabs 67-71 synuclein alpha Homo sapiens 131-139 34020303-9 2021 CONCLUSIONS: Differences in the plasma/CSF distribution of anti-alpha-syn nAbs seem to be a common feature of synucleinopathies. nabs 74-78 synuclein alpha Homo sapiens 64-73 34020303-2 2021 Recently, we reported reduced high-affinity/avidity anti-alpha-syn nAbs levels in plasma from MSA and PD patients, along with distinct inter-group immunoglobulin (Ig)G subclass distributions. nabs 67-71 synuclein alpha Homo sapiens 57-66 28592329-5 2017 METHODS: We have investigated the apparent affinity of anti-alpha-synuclein NAbs in plasma samples from 46 PD patients, 18 MSA patients and 41 controls using competitive enzyme-linked immunosorbent assay (ELISA) and Meso Scale Discovery (MSD) set-ups. nabs 76-80 synuclein alpha Homo sapiens 60-75 30481547-5 2019 Compared with vehicles, NAbs-alpha-syn significantly attenuated the memory and motor deficits by reducing the levels of soluble alpha-syn, total human alpha-syn and alpha-syn oligomers, decreasing the intracellular p-alpha-synser129 deposits and axonal pathology, inhibiting the microgliosis and astrogliosis, as well as the production of proinflammatory cytokines, increasing the levels of PSD95, synaptophysin and TH in the brain of A53T transgenic mice. nabs 24-28 synuclein alpha Homo sapiens 29-38 30481547-5 2019 Compared with vehicles, NAbs-alpha-syn significantly attenuated the memory and motor deficits by reducing the levels of soluble alpha-syn, total human alpha-syn and alpha-syn oligomers, decreasing the intracellular p-alpha-synser129 deposits and axonal pathology, inhibiting the microgliosis and astrogliosis, as well as the production of proinflammatory cytokines, increasing the levels of PSD95, synaptophysin and TH in the brain of A53T transgenic mice. nabs 24-28 synuclein alpha Homo sapiens 128-137 30481547-5 2019 Compared with vehicles, NAbs-alpha-syn significantly attenuated the memory and motor deficits by reducing the levels of soluble alpha-syn, total human alpha-syn and alpha-syn oligomers, decreasing the intracellular p-alpha-synser129 deposits and axonal pathology, inhibiting the microgliosis and astrogliosis, as well as the production of proinflammatory cytokines, increasing the levels of PSD95, synaptophysin and TH in the brain of A53T transgenic mice. nabs 24-28 synuclein alpha Homo sapiens 128-137 30481547-5 2019 Compared with vehicles, NAbs-alpha-syn significantly attenuated the memory and motor deficits by reducing the levels of soluble alpha-syn, total human alpha-syn and alpha-syn oligomers, decreasing the intracellular p-alpha-synser129 deposits and axonal pathology, inhibiting the microgliosis and astrogliosis, as well as the production of proinflammatory cytokines, increasing the levels of PSD95, synaptophysin and TH in the brain of A53T transgenic mice. nabs 24-28 synuclein alpha Homo sapiens 128-137 29306403-6 2018 The presence of alpha-syn and tau reactive autoantibodies in early childhood indicates that both immunoglobulins belong to the pool of naturally occurring autoantibodies (nAbs), as their antigen-independent synthesis from birth is a crucial characteristic. nabs 171-175 synuclein alpha Homo sapiens 16-25 30954607-6 2019 Cotreatment with nAbs alpha-Syn alleviated the release of pro-inflammatory cytokines induced by alpha-Syn fragments alpha-Syn 1-95, alpha-Syn 61-140, alpha-Syn 96-140 and alpha-Syn 112. nabs 17-21 synuclein alpha Homo sapiens 22-31 28592329-8 2017 Further, cross binding of anti-alpha-synuclein NAbs with beta- and gamma-synuclein monomers suggest, the high affinity anti-alpha-synuclein plasma component, seen in healthy individuals, is directed mainly against C-terminal epitopes. nabs 47-51 synuclein alpha Homo sapiens 31-46 28592329-8 2017 Further, cross binding of anti-alpha-synuclein NAbs with beta- and gamma-synuclein monomers suggest, the high affinity anti-alpha-synuclein plasma component, seen in healthy individuals, is directed mainly against C-terminal epitopes. nabs 47-51 synuclein alpha Homo sapiens 124-139 28592329-9 2017 Furthermore, we also observed reduced occurrence of high affinity anti-phosphorylated-alpha-synuclein NAbs in plasma from PD and MSA patients. nabs 102-106 synuclein alpha Homo sapiens 86-101 28592329-10 2017 CONCLUSIONS: One interpretation implies that these patients may have impaired ability to clear and/or block the effects of pathological alpha-synuclein due to insufficient/absent concentration of NAbs and as such provides a rationale for testing immune-based therapeutic strategies directed against pathological alpha-synuclein. nabs 196-200 synuclein alpha Homo sapiens 136-151