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Differential effects between γ-secretase inhibitors and modulators on cognitive function in amyloid precursor protein-transgenic and nontransgenic mice.

Mitani Y, Yarimizu J, Saita K, Uchino H, Akashiba H, Shitaka Y, Ni K, Matsuoka N.

J Neurosci. 2012 Feb 8;32(6):2037-50. doi: 10.1523/JNEUROSCI.4264-11.2012.


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.


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.


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.


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.


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.


The genetics of Alzheimer disease: back to the future.

Bertram L, Lill CM, Tanzi RE.

Neuron. 2010 Oct 21;68(2):270-81. doi: 10.1016/j.neuron.2010.10.013. Review.


The secretases: enzymes with therapeutic potential in Alzheimer disease.

De Strooper B, Vassar R, Golde T.

Nat Rev Neurol. 2010 Feb;6(2):99-107. doi: 10.1038/nrneurol.2009.218. Review.


Generation and initial characterization of FDD knock in mice.

Giliberto L, Matsuda S, Vidal R, D'Adamio L.

PLoS One. 2009 Nov 18;4(11):e7900. doi: 10.1371/journal.pone.0007900.


Maturation of BRI2 generates a specific inhibitor that reduces APP processing at the plasma membrane and in endocytic vesicles.

Matsuda S, Matsuda Y, Snapp EL, D'Adamio L.

Neurobiol Aging. 2011 Aug;32(8):1400-8. doi: 10.1016/j.neurobiolaging.2009.08.005.


Presenilins are essential for regulating neurotransmitter release.

Zhang C, Wu B, Beglopoulos V, Wines-Samuelson M, Zhang D, Dragatsis I, Südhof TC, Shen J.

Nature. 2009 Jul 30;460(7255):632-6. doi: 10.1038/nature08177.


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.


The Alzheimer's disease beta-secretase enzyme, BACE1.

Cole SL, Vassar R.

Mol Neurodegener. 2007 Nov 15;2:22.


The presenilin hypothesis of Alzheimer's disease: evidence for a loss-of-function pathogenic mechanism.

Shen J, Kelleher RJ 3rd.

Proc Natl Acad Sci U S A. 2007 Jan 9;104(2):403-9. Review.


BRI2 interacts with amyloid precursor protein (APP) and regulates amyloid beta (Abeta) production.

Fotinopoulou A, Tsachaki M, Vlavaki M, Poulopoulos A, Rostagno A, Frangione B, Ghiso J, Efthimiopoulos S.

J Biol Chem. 2005 Sep 2;280(35):30768-72.


The familial dementia BRI2 gene binds the Alzheimer gene amyloid-beta precursor protein and inhibits amyloid-beta production.

Matsuda S, Giliberto L, Matsuda Y, Davies P, McGowan E, Pickford F, Ghiso J, Frangione B, D'Adamio L.

J Biol Chem. 2005 Aug 12;280(32):28912-6.


Molecular biology and genetics of Alzheimer's disease.

St George-Hyslop PH, Petit A.

C R Biol. 2005 Feb;328(2):119-30. Review.

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