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Items: 1 to 20 of 499

1.

Prion-like behaviour and tau-dependent cytotoxicity of pyroglutamylated amyloid-β.

Nussbaum JM, Schilling S, Cynis H, Silva A, Swanson E, Wangsanut T, Tayler K, Wiltgen B, Hatami A, Rönicke R, Reymann K, Hutter-Paier B, Alexandru A, Jagla W, Graubner S, Glabe CG, Demuth HU, Bloom GS.

Nature. 2012 May 2;485(7400):651-5. doi: 10.1038/nature11060.

2.

Pyroglutamylated amyloid-β peptide reverses cross β-sheets by a prion-like mechanism.

Matos JO, Goldblatt G, Jeon J, Chen B, Tatulian SA.

J Phys Chem B. 2014 May 29;118(21):5637-43. doi: 10.1021/jp412743s.

3.

Pyroglutamylated amyloid-β is associated with hyperphosphorylated tau and severity of Alzheimer's disease.

Mandler M, Walker L, Santic R, Hanson P, Upadhaya AR, Colloby SJ, Morris CM, Thal DR, Thomas AJ, Schneeberger A, Attems J.

Acta Neuropathol. 2014 Jul;128(1):67-79. doi: 10.1007/s00401-014-1296-9.

PMID:
24861310
4.

Co-occurrence of Alzheimer's disease ß-amyloid and τ pathologies at synapses.

Takahashi RH, Capetillo-Zarate E, Lin MT, Milner TA, Gouras GK.

Neurobiol Aging. 2010 Jul;31(7):1145-52. doi: 10.1016/j.neurobiolaging.2008.07.021.

5.

Beta-amyloid1-42 gene transfer model exhibits intraneuronal amyloid, gliosis, tau phosphorylation, and neuronal loss.

Rebeck GW, Hoe HS, Moussa CE.

J Biol Chem. 2010 Mar 5;285(10):7440-6. doi: 10.1074/jbc.M109.083915.

6.

Systemic vaccination with anti-oligomeric monoclonal antibodies improves cognitive function by reducing Aβ deposition and tau pathology in 3xTg-AD mice.

Rasool S, Martinez-Coria H, Wu JW, LaFerla F, Glabe CG.

J Neurochem. 2013 Aug;126(4):473-82. doi: 10.1111/jnc.12305.

7.

[Alzheimer disease: cellular and molecular aspects].

Octave JN.

Bull Mem Acad R Med Belg. 2005;160(10-12):445-9; discussion 450-1. French.

PMID:
16768248
8.

Abeta exacerbates the neuronal dysfunction caused by human tau expression in a Drosophila model of Alzheimer's disease.

Folwell J, Cowan CM, Ubhi KK, Shiabh H, Newman TA, Shepherd D, Mudher A.

Exp Neurol. 2010 Jun;223(2):401-9. doi: 10.1016/j.expneurol.2009.09.014.

PMID:
19782075
9.

Alzheimer's disease.

De-Paula VJ, Radanovic M, Diniz BS, Forlenza OV.

Subcell Biochem. 2012;65:329-52. doi: 10.1007/978-94-007-5416-4_14. Review.

PMID:
23225010
10.

Amyloid-β and tau: the trigger and bullet in Alzheimer disease pathogenesis.

Bloom GS.

JAMA Neurol. 2014 Apr;71(4):505-8. doi: 10.1001/jamaneurol.2013.5847. Review.

PMID:
24493463
11.

Alzheimer disease: a tale of two prions.

Nussbaum JM, Seward ME, Bloom GS.

Prion. 2013 Jan-Feb;7(1):14-9. doi: 10.4161/pri.22118. Review.

12.

A physically-modified saline suppresses neuronal apoptosis, attenuates tau phosphorylation and protects memory in an animal model of Alzheimer's disease.

Modi KK, Jana A, Ghosh S, Watson R, Pahan K.

PLoS One. 2014 Aug 4;9(8):e103606. doi: 10.1371/journal.pone.0103606.

13.

The novel calpain inhibitor A-705253 potently inhibits oligomeric beta-amyloid-induced dynamin 1 and tau cleavage in hippocampal neurons.

Sinjoanu RC, Kleinschmidt S, Bitner RS, Brioni JD, Moeller A, Ferreira A.

Neurochem Int. 2008 Sep;53(3-4):79-88. doi: 10.1016/j.neuint.2008.06.003.

14.

Role of PrP(C) Expression in Tau Protein Levels and Phosphorylation in Alzheimer's Disease Evolution.

Vergara C, Ordóñez-Gutiérrez L, Wandosell F, Ferrer I, del Río JA, Gavín R.

Mol Neurobiol. 2015;51(3):1206-20. doi: 10.1007/s12035-014-8793-7.

PMID:
24965601
15.

Amyloid-induced neurofibrillary tangle formation in Alzheimer's disease: insight from transgenic mouse and tissue-culture models.

Götz J, Schild A, Hoerndli F, Pennanen L.

Int J Dev Neurosci. 2004 Nov;22(7):453-65. Review.

PMID:
15465275
16.

Pharmacological modulation of GSAP reduces amyloid-β levels and tau phosphorylation in a mouse model of Alzheimer's disease with plaques and tangles.

Chu J, Lauretti E, Craige CP, Praticò D.

J Alzheimers Dis. 2014;41(3):729-37. doi: 10.3233/JAD-140105.

PMID:
24662099
17.

Brain amyloid-β oligomers in ageing and Alzheimer's disease.

Lesné SE, Sherman MA, Grant M, Kuskowski M, Schneider JA, Bennett DA, Ashe KH.

Brain. 2013 May;136(Pt 5):1383-98. doi: 10.1093/brain/awt062.

18.
19.

Low-n oligomers as therapeutic targets of Alzheimer's disease.

Ono K, Yamada M.

J Neurochem. 2011 Apr;117(1):19-28. doi: 10.1111/j.1471-4159.2011.07187.x. Review.

20.

Accumulation of intraneuronal β-amyloid 42 peptides is associated with early changes in microtubule-associated protein 2 in neurites and synapses.

Takahashi RH, Capetillo-Zarate E, Lin MT, Milner TA, Gouras GK.

PLoS One. 2013;8(1):e51965. doi: 10.1371/journal.pone.0051965.

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