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Major prion protein: Difference between revisions

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==== Memory ====
 
While null mice exhibit normal learning ability and [[short-term memory]], [[long-term memory]] consolidation deficits have been demonstrated. As with [[ataxia]], however, this is attributable to Doppel gene expression. However, [[spatial learning]], a predominantly hippocampal-function, is decreased in the null mice and can be recovered with the reinstatement of PrP in neurons; this indicates that loss of PrP function is the cause.<ref name = "pmid15837581">{{cite journal | vauthors = Criado JR, Sánchez-Alavez M, Conti B, Giacchino JL, Wills DN, Henriksen SJ, Race R, Manson JC, Chesebro B, Oldstone MB | title = Mice devoid of prion protein have cognitive deficits that are rescued by reconstitution of PrP in neurons | journal = Neurobiol. Dis. | volume = 19 | issue = 1–2 | pages = 255–65 | year = 2005 | pmid = 15837581 | doi = 10.1016/j.nbd.2005.01.001| s2cid = 2618712 }}</ref><ref name = "pmid20133875">{{cite journal | vauthors = Balducci C, Beeg M, Stravalaci M, Bastone A, Sclip A, Biasini E, Tapella L, Colombo L, Manzoni C, Borsello T, Chiesa R, Gobbi M, Salmona M, Forloni G | title = Synthetic amyloid-beta oligomers impair long-term memory independently of cellular prion protein | journal = Proc. Natl. Acad. Sci. U.S.A. | volume = 107 | issue = 5 | pages = 2295–300 | date = February 2010 | pmid = 20133875 | pmc = 2836680 | doi = 10.1073/pnas.0911829107| bibcode = 2010PNAS..107.2295B | doi-access = free }}</ref> The interaction of hippocampal PrP with [[laminin]] (LN) is pivotal in memory processing and is likely modulated by the [[kinases]] PKA and ERK1/2.<ref name = "pmid17156386">{{cite journal | vauthors = Coitinho AS, Freitas AR, Lopes MH, Hajj GN, Roesler R, Walz R, Rossato JI, Cammarota M, Izquierdo I, Martins VR, Brentani RR | title = The interaction between prion protein and laminin modulates memory consolidation | journal = Eur. J. Neurosci. | volume = 24 | issue = 11 | pages = 3255–64 | date = December 2006 | pmid = 17156386 | doi = 10.1111/j.1460-9568.2006.05156.x| s2cid = 17164351 }}</ref><ref name = "pmid15931169">{{cite journal | vauthors = Shorter J, Lindquist S | title = Prions as adaptive conduits of memory and inheritance | journal = Nat. Rev. Genet. | volume = 6 | issue = 6 | pages = 435–50 | date = June 2005 | pmid = 15931169 | doi = 10.1038/nrg1616| s2cid = 5575951 }}</ref>
 
Further support for PrP's role in memory formation is derived from several population studies. A test of healthy young humans showed increased long-term memory ability associated with an MM or MV genotype when compared to VV.<ref name = "pmid15987701">{{cite journal | vauthors = Papassotiropoulos A, Wollmer MA, Aguzzi A, Hock C, Nitsch RM, de Quervain DJ | title = The prion gene is associated with human long-term memory | journal = Hum. Mol. Genet. | volume = 14 | issue = 15 | pages = 2241–6 | date = August 2005 | pmid = 15987701 | doi = 10.1093/hmg/ddi228| url = http://doc.rero.ch/record/297873/files/ddi228.pdf | doi-access = free }}</ref> [[Down syndrome]] patients with a single [[valine]] substitution have been linked to earlier cognitive decline.<ref name = "pmid12796830">{{cite journal | vauthors = Del Bo R, Comi GP, Giorda R, Crimi M, Locatelli F, Martinelli-Boneschi F, Pozzoli U, Castelli E, Bresolin N, Scarlato G | title = The 129 codon polymorphism of the prion protein gene influences earlier cognitive performance in Down syndrome subjects | journal = J. Neurol. | volume = 250 | issue = 6 | pages = 688–92 | date = June 2003 | pmid = 12796830 | doi = 10.1007/s00415-003-1057-5| s2cid = 21049364 }}</ref> Several [[Polymorphism (biology)|polymorphisms]] in ''PRNP'' have been linked with cognitive impairment in the elderly as well as earlier cognitive decline.<ref name = "pmid9748018">{{cite journal | vauthors = Berr C, Richard F, Dufouil C, Amant C, Alperovitch A, Amouyel P | title = Polymorphism of the prion protein is associated with cognitive impairment in the elderly: the EVA study | journal = Neurology | volume = 51 | issue = 3 | pages = 734–7 | date = September 1998 | pmid = 9748018 | doi = 10.1212/wnl.51.3.734| s2cid = 11352163 }}</ref><ref name = "pmid12891686">{{cite journal | vauthors = Croes EA, Dermaut B, Houwing-Duistermaat JJ, Van den Broeck M, Cruts M, Breteler MM, Hofman A, van Broeckhoven C, van Duijn CM | title = Early cognitive decline is associated with prion protein codon 129 polymorphism | journal = Ann. Neurol. | volume = 54 | issue = 2 | pages = 275–6 | date = August 2003 | pmid = 12891686 | doi = 10.1002/ana.10658| s2cid = 31538672 }}</ref><ref name = "pmid16023289">{{cite journal | vauthors = Kachiwala SJ, Harris SE, Wright AF, Hayward C, Starr JM, Whalley LJ, Deary IJ | title = Genetic influences on oxidative stress and their association with normal cognitive ageing | journal = Neurosci. Lett. | volume = 386 | issue = 2 | pages = 116–20 | date = September 2005 | pmid = 16023289 | doi = 10.1016/j.neulet.2005.05.067| s2cid = 23642220 }}</ref> All of these studies investigated differences in codon 129, indicating its importance in the overall functionality of PrP, in particular with regard to memory.
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