Quantum redactiones paginae "Proteinum praecursor amyloidi" differant

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Incrementum [[glutamatum|glutamati]] extracellularis influxum [[calium|calcii]] extracellularis (Ca<sup>2+</sup>) in cellulam incitat, quod damnum neurotoxicum perficere potest. Liberatum sAPP alpha sane transgressionem Ca<sup>2+</sup> hanc in cellulam supprimit<ref>{{cite journal |authors=Furukawa K., Mattson M. P. |title=Secreted amyloid precursor protein alpha selectively suppresses N-methyl-D-aspartate currents in hippocampal neurons: involvement of cyclic GMP |journal=Neuroscience |year=1998 |month=Mar |volume=83 |issue=2 |pages=429-38 |url=https://www.ncbi.nlm.nih.gov/pubmed/9460751}}</ref>. Per [[cyclicum guanosinum monophosphatum]] (cGMP) [[receptorium NMDA|receptoria NMDA]] ([[neurotransmissor]]is glutamati excitantis) pariter inhibentur ("neuroprotectio").
 
Praeterea proteino praecursori munera equilibrii ferri (egressionis Fe<sup>2+</sup>) habet, pariter ut [[enzymum]] [[caeruloplasminum]] in cellulis extra neurones (quibus non invenitur)<ref>{{cite journal |authors=Wong B. X., Tsatsanis A., Lim L. Q., Adlard P. A., Bush A. I., Duce J. A. |title=β-Amyloid precursor protein does not possess ferroxidase activity but does stabilize the cell surface ferrous iron exporter ferroportin |journal=PloS one |year=2014 |month=Dec |volume=9 |issue=12 |pages=e114174 |url=https://www.ncbi.nlm.nih.gov/pubmed/25464026/}}</ref>.
 
== Pathophysiologia et neuropathologia ==