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Results: 1 to 20 of 92

Similar articles for PubMed (Select 22514310)

1.

Memory deficits of British dementia knock-in mice are prevented by Aβ-precursor protein haploinsufficiency.

Tamayev R, D'Adamio L.

J Neurosci. 2012 Apr 18;32(16):5481-5. doi: 10.1523/JNEUROSCI.5193-11.2012.

2.

APP heterozygosity averts memory deficit in knockin mice expressing the Danish dementia BRI2 mutant.

Tamayev R, Matsuda S, Giliberto L, Arancio O, D'Adamio L.

EMBO J. 2011 May 17;30(12):2501-9. doi: 10.1038/emboj.2011.161.

3.

Memory deficits due to familial British dementia BRI2 mutation are caused by loss of BRI2 function rather than amyloidosis.

Tamayev R, Giliberto L, Li W, d'Abramo C, Arancio O, Vidal R, D'Adamio L.

J Neurosci. 2010 Nov 3;30(44):14915-24. doi: 10.1523/JNEUROSCI.3917-10.2010.

4.

Increased AβPP processing in familial Danish dementia patients.

Matsuda S, Tamayev R, D'Adamio L.

J Alzheimers Dis. 2011;27(2):385-91. doi: 10.3233/JAD-2011-110785.

5.

Role of BRI2 in dementia.

Del Campo M, Teunissen CE.

J Alzheimers Dis. 2014;40(3):481-94. doi: 10.3233/JAD-131364. Review.

PMID:
24473189
6.

Inhibition of γ-secretase worsens memory deficits in a genetically congruous mouse model of Danish dementia.

Tamayev R, D'Adamio L.

Mol Neurodegener. 2012 Apr 26;7:19. doi: 10.1186/1750-1326-7-19.

7.

β- but not γ-secretase proteolysis of APP causes synaptic and memory deficits in a mouse model of dementia.

Tamayev R, Matsuda S, Arancio O, D'Adamio L.

EMBO Mol Med. 2012 Mar;4(3):171-9. doi: 10.1002/emmm.201100195. Epub 2012 Jan 23.

8.

Caspase-9 mediates synaptic plasticity and memory deficits of Danish dementia knock-in mice: caspase-9 inhibition provides therapeutic protection.

Tamayev R, Akpan N, Arancio O, Troy CM, D'Adamio L.

Mol Neurodegener. 2012 Dec 10;7:60. doi: 10.1186/1750-1326-7-60.

9.

Danish dementia mice suggest that loss of function and not the amyloid cascade causes synaptic plasticity and memory deficits.

Tamayev R, Matsuda S, Fà M, Arancio O, D'Adamio L.

Proc Natl Acad Sci U S A. 2010 Nov 30;107(48):20822-7. doi: 10.1073/pnas.1011689107. Epub 2010 Nov 22.

10.

Conditional inactivation of presenilin 1 prevents amyloid accumulation and temporarily rescues contextual and spatial working memory impairments in amyloid precursor protein transgenic mice.

Saura CA, Chen G, Malkani S, Choi SY, Takahashi RH, Zhang D, Gouras GK, Kirkwood A, Morris RG, Shen J.

J Neurosci. 2005 Jul 20;25(29):6755-64.

11.

BRI2 (ITM2b) inhibits Abeta deposition in vivo.

Kim J, Miller VM, Levites Y, West KJ, Zwizinski CW, Moore BD, Troendle FJ, Bann M, Verbeeck C, Price RW, Smithson L, Sonoda L, Wagg K, Rangachari V, Zou F, Younkin SG, Graff-Radford N, Dickson D, Rosenberry T, Golde TE.

J Neurosci. 2008 Jun 4;28(23):6030-6. doi: 10.1523/JNEUROSCI.0891-08.2008.

12.

An intracellular threonine of amyloid-β precursor protein mediates synaptic plasticity deficits and memory loss.

Lombino F, Biundo F, Tamayev R, Arancio O, D'Adamio L.

PLoS One. 2013;8(2):e57120. doi: 10.1371/journal.pone.0057120. Epub 2013 Feb 22.

13.

Expression of BRI2 mRNA and protein in normal human brain and familial British dementia: its relevance to the pathogenesis of disease.

Lashley T, Revesz T, Plant G, Bandopadhyay R, Lees AJ, Frangione B, Wood NW, de Silva R, Ghiso J, Rostagno A, Holton JL.

Neuropathol Appl Neurobiol. 2008 Oct;34(5):492-505. doi: 10.1111/j.1365-2990.2008.00935.x. Epub 2008 Feb 13.

14.

BRI2 inhibits amyloid beta-peptide precursor protein processing by interfering with the docking of secretases to the substrate.

Matsuda S, Giliberto L, Matsuda Y, McGowan EM, D'Adamio L.

J Neurosci. 2008 Aug 27;28(35):8668-76. doi: 10.1523/JNEUROSCI.2094-08.2008.

15.

BRI2 protein regulates β-amyloid degradation by increasing levels of secreted insulin-degrading enzyme (IDE).

Kilger E, Buehler A, Woelfing H, Kumar S, Kaeser SA, Nagarathinam A, Walter J, Jucker M, Coomaraswamy J.

J Biol Chem. 2011 Oct 28;286(43):37446-57. doi: 10.1074/jbc.M111.288373. Epub 2011 Aug 26.

16.

Ryanodine receptor blockade reduces amyloid-β load and memory impairments in Tg2576 mouse model of Alzheimer disease.

Oulès B, Del Prete D, Greco B, Zhang X, Lauritzen I, Sevalle J, Moreno S, Paterlini-Bréchot P, Trebak M, Checler F, Benfenati F, Chami M.

J Neurosci. 2012 Aug 22;32(34):11820-34.

17.

Amyloid peptides ABri and ADan show differential neurotoxicity in transgenic Drosophila models of familial British and Danish dementia.

Marcora MS, Fernández-Gamba AC, Avendaño LA, Rotondaro C, Podhajcer OL, Vidal R, Morelli L, Ceriani MF, Castaño EM.

Mol Neurodegener. 2014 Jan 9;9:5. doi: 10.1186/1750-1326-9-5.

18.
19.

Reversible pathologic and cognitive phenotypes in an inducible model of Alzheimer-amyloidosis.

Melnikova T, Fromholt S, Kim H, Lee D, Xu G, Price A, Moore BD, Golde TE, Felsenstein KM, Savonenko A, Borchelt DR.

J Neurosci. 2013 Feb 27;33(9):3765-79. doi: 10.1523/JNEUROSCI.4251-12.2013.

20.

Temporal memory deficits in Alzheimer's mouse models: rescue by genetic deletion of BACE1.

Ohno M, Chang L, Tseng W, Oakley H, Citron M, Klein WL, Vassar R, Disterhoft JF.

Eur J Neurosci. 2006 Jan;23(1):251-60.

PMID:
16420434
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