PMC:6710390 / 8147-9295 JSONTXT

{"project":"2_test","denotations":[{"id":"31481869-19176820-38391681","span":{"begin":125,"end":129},"obj":"19176820"},{"id":"31481869-19176820-38391682","span":{"begin":476,"end":480},"obj":"19176820"},{"id":"31481869-19176820-38391683","span":{"begin":600,"end":604},"obj":"19176820"},{"id":"31481869-21346312-38391684","span":{"begin":757,"end":761},"obj":"21346312"},{"id":"31481869-23358924-38391685","span":{"begin":778,"end":782},"obj":"23358924"},{"id":"31481869-23358924-38391686","span":{"begin":1142,"end":1146},"obj":"23358924"}],"text":"Sporadic AD is mainly caused by an imbalance between Aβ production and clearance, resulting in Aβ accumulation. Rose et al. (2009) elucidated the effect of NPY on Aβ in AD. NPY C-terminal fragments (CTFs) were cleaved from full-length NPY by extracellular endopeptidase neprilysin. This generated a prominent CTF comprising amino acids 21–36 and 31–36. Infusion of these NPY CTFs into the brains of mouse models of AD ameliorated the neurodegenerative pathology (Rose et al., 2009). In addition, the amidated NPY CTFs protected human neuronal cultures from the neurotoxic effects of Aβ (Rose et al., 2009). NPY did not only have an effect on offsetting the toxic effect of Aβ, but also restored the neurotrophin levels in neuroblastoma cells (Croce et al., 2011). Croce et al. (2013) pre-incubated primary rat cortical neurons with NPY and exposed them to Aβ25–35 fragments. They found that NPY mediated a decrease in miR-30a-5p expression and an increase in brain derived neurotrophic factor (BDNF) mRNA and protein levels, which possibly contributed to the neuroprotective effect of NPY in rat cortical neurons exposed to Aβ (Croce et al., 2013)."}

{"project":"TEST0","denotations":[{"id":"31481869-13-21-481188","span":{"begin":125,"end":129},"obj":"[\"19176820\"]"},{"id":"31481869-123-131-481189","span":{"begin":476,"end":480},"obj":"[\"19176820\"]"},{"id":"31481869-117-125-481190","span":{"begin":600,"end":604},"obj":"[\"19176820\"]"},{"id":"31481869-150-158-481191","span":{"begin":757,"end":761},"obj":"[\"21346312\"]"},{"id":"31481869-14-22-481192","span":{"begin":778,"end":782},"obj":"[\"23358924\"]"},{"id":"31481869-227-235-481193","span":{"begin":1142,"end":1146},"obj":"[\"23358924\"]"}],"text":"Sporadic AD is mainly caused by an imbalance between Aβ production and clearance, resulting in Aβ accumulation. Rose et al. (2009) elucidated the effect of NPY on Aβ in AD. NPY C-terminal fragments (CTFs) were cleaved from full-length NPY by extracellular endopeptidase neprilysin. This generated a prominent CTF comprising amino acids 21–36 and 31–36. Infusion of these NPY CTFs into the brains of mouse models of AD ameliorated the neurodegenerative pathology (Rose et al., 2009). In addition, the amidated NPY CTFs protected human neuronal cultures from the neurotoxic effects of Aβ (Rose et al., 2009). NPY did not only have an effect on offsetting the toxic effect of Aβ, but also restored the neurotrophin levels in neuroblastoma cells (Croce et al., 2011). Croce et al. (2013) pre-incubated primary rat cortical neurons with NPY and exposed them to Aβ25–35 fragments. They found that NPY mediated a decrease in miR-30a-5p expression and an increase in brain derived neurotrophic factor (BDNF) mRNA and protein levels, which possibly contributed to the neuroprotective effect of NPY in rat cortical neurons exposed to Aβ (Croce et al., 2013)."}

{"project":"0_colil","denotations":[{"id":"31481869-19176820-481188","span":{"begin":125,"end":129},"obj":"19176820"},{"id":"31481869-19176820-481189","span":{"begin":476,"end":480},"obj":"19176820"},{"id":"31481869-19176820-481190","span":{"begin":600,"end":604},"obj":"19176820"},{"id":"31481869-21346312-481191","span":{"begin":757,"end":761},"obj":"21346312"},{"id":"31481869-23358924-481192","span":{"begin":778,"end":782},"obj":"23358924"},{"id":"31481869-23358924-481193","span":{"begin":1142,"end":1146},"obj":"23358924"}],"text":"Sporadic AD is mainly caused by an imbalance between Aβ production and clearance, resulting in Aβ accumulation. Rose et al. (2009) elucidated the effect of NPY on Aβ in AD. NPY C-terminal fragments (CTFs) were cleaved from full-length NPY by extracellular endopeptidase neprilysin. This generated a prominent CTF comprising amino acids 21–36 and 31–36. Infusion of these NPY CTFs into the brains of mouse models of AD ameliorated the neurodegenerative pathology (Rose et al., 2009). In addition, the amidated NPY CTFs protected human neuronal cultures from the neurotoxic effects of Aβ (Rose et al., 2009). NPY did not only have an effect on offsetting the toxic effect of Aβ, but also restored the neurotrophin levels in neuroblastoma cells (Croce et al., 2011). Croce et al. (2013) pre-incubated primary rat cortical neurons with NPY and exposed them to Aβ25–35 fragments. They found that NPY mediated a decrease in miR-30a-5p expression and an increase in brain derived neurotrophic factor (BDNF) mRNA and protein levels, which possibly contributed to the neuroprotective effect of NPY in rat cortical neurons exposed to Aβ (Croce et al., 2013)."}