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Items: 1 to 20 of 149

1.

Defective lysosomal proteolysis and axonal transport are early pathogenic events that worsen with age leading to increased APP metabolism and synaptic Abeta in transgenic APP/PS1 hippocampus.

Torres M, Jimenez S, Sanchez-Varo R, Navarro V, Trujillo-Estrada L, Sanchez-Mejias E, Carmona I, Davila JC, Vizuete M, Gutierrez A, Vitorica J.

Mol Neurodegener. 2012 Nov 22;7:59. doi: 10.1186/1750-1326-7-59.

2.

Abnormal accumulation of autophagic vesicles correlates with axonal and synaptic pathology in young Alzheimer's mice hippocampus.

Sanchez-Varo R, Trujillo-Estrada L, Sanchez-Mejias E, Torres M, Baglietto-Vargas D, Moreno-Gonzalez I, De Castro V, Jimenez S, Ruano D, Vizuete M, Davila JC, Garcia-Verdugo JM, Jimenez AJ, Vitorica J, Gutierrez A.

Acta Neuropathol. 2012 Jan;123(1):53-70. doi: 10.1007/s00401-011-0896-x. Epub 2011 Oct 22.

3.

Neuronal-Targeted TFEB Accelerates Lysosomal Degradation of APP, Reducing Aβ Generation and Amyloid Plaque Pathogenesis.

Xiao Q, Yan P, Ma X, Liu H, Perez R, Zhu A, Gonzales E, Tripoli DL, Czerniewski L, Ballabio A, Cirrito JR, Diwan A, Lee JM.

J Neurosci. 2015 Sep 2;35(35):12137-51. doi: 10.1523/JNEUROSCI.0705-15.2015.

4.

Protective effects of positive lysosomal modulation in Alzheimer's disease transgenic mouse models.

Butler D, Hwang J, Estick C, Nishiyama A, Kumar SS, Baveghems C, Young-Oxendine HB, Wisniewski ML, Charalambides A, Bahr BA.

PLoS One. 2011;6(6):e20501. doi: 10.1371/journal.pone.0020501. Epub 2011 Jun 10.

5.

Early alterations in energy metabolism in the hippocampus of APPswe/PS1dE9 mouse model of Alzheimer's disease.

Pedrós I, Petrov D, Allgaier M, Sureda F, Barroso E, Beas-Zarate C, Auladell C, Pallàs M, Vázquez-Carrera M, Casadesús G, Folch J, Camins A.

Biochim Biophys Acta. 2014 Sep;1842(9):1556-66. doi: 10.1016/j.bbadis.2014.05.025. Epub 2014 Jun 2.

6.

Amyloid precursor protein-induced axonopathies are independent of amyloid-beta peptides.

Stokin GB, Almenar-Queralt A, Gunawardena S, Rodrigues EM, Falzone T, Kim J, Lillo C, Mount SL, Roberts EA, McGowan E, Williams DS, Goldstein LS.

Hum Mol Genet. 2008 Nov 15;17(22):3474-86. doi: 10.1093/hmg/ddn240. Epub 2008 Aug 11.

7.

The β-secretase-derived C-terminal fragment of βAPP, C99, but not Aβ, is a key contributor to early intraneuronal lesions in triple-transgenic mouse hippocampus.

Lauritzen I, Pardossi-Piquard R, Bauer C, Brigham E, Abraham JD, Ranaldi S, Fraser P, St-George-Hyslop P, Le Thuc O, Espin V, Chami L, Dunys J, Checler F.

J Neurosci. 2012 Nov 14;32(46):16243-55a. doi: 10.1523/JNEUROSCI.2775-12.2012.

8.
9.

Amyloid precursor protein processing and retinal pathology in mouse models of Alzheimer's disease.

Dutescu RM, Li QX, Crowston J, Masters CL, Baird PN, Culvenor JG.

Graefes Arch Clin Exp Ophthalmol. 2009 Sep;247(9):1213-21. doi: 10.1007/s00417-009-1060-3. Epub 2009 Mar 7.

PMID:
19271231
10.

Neuronal deficiency of presenilin 1 inhibits amyloid plaque formation and corrects hippocampal long-term potentiation but not a cognitive defect of amyloid precursor protein [V717I] transgenic mice.

Dewachter I, Reversé D, Caluwaerts N, Ris L, Kuipéri C, Van den Haute C, Spittaels K, Umans L, Serneels L, Thiry E, Moechars D, Mercken M, Godaux E, Van Leuven F.

J Neurosci. 2002 May 1;22(9):3445-53.

11.

Treadmill exercise enhances synaptic plasticity, but does not alter β-amyloid deposition in hippocampi of aged APP/PS1 transgenic mice.

Zhao G, Liu HL, Zhang H, Tong XJ.

Neuroscience. 2015 Jul 9;298:357-66. doi: 10.1016/j.neuroscience.2015.04.038. Epub 2015 Apr 23.

PMID:
25917310
12.

APP/PS1 mice overexpressing SREBP-2 exhibit combined Aβ accumulation and tau pathology underlying Alzheimer's disease.

Barbero-Camps E, Fernández A, Martínez L, Fernández-Checa JC, Colell A.

Hum Mol Genet. 2013 Sep 1;22(17):3460-76. doi: 10.1093/hmg/ddt201. Epub 2013 May 6.

13.

TUDCA, a bile acid, attenuates amyloid precursor protein processing and amyloid-β deposition in APP/PS1 mice.

Nunes AF, Amaral JD, Lo AC, Fonseca MB, Viana RJ, Callaerts-Vegh Z, D'Hooge R, Rodrigues CM.

Mol Neurobiol. 2012 Jun;45(3):440-54. doi: 10.1007/s12035-012-8256-y. Epub 2012 Mar 23.

PMID:
22438081
14.

APP transgenic modeling of Alzheimer's disease: mechanisms of neurodegeneration and aberrant neurogenesis.

Crews L, Rockenstein E, Masliah E.

Brain Struct Funct. 2010 Mar;214(2-3):111-26. doi: 10.1007/s00429-009-0232-6. Epub 2009 Nov 29. Review.

15.

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
16.

Long-term treadmill exercise inhibits the progression of Alzheimer's disease-like neuropathology in the hippocampus of APP/PS1 transgenic mice.

Liu HL, Zhao G, Zhang H, Shi LD.

Behav Brain Res. 2013 Nov 1;256:261-72. doi: 10.1016/j.bbr.2013.08.008. Epub 2013 Aug 19.

PMID:
23968591
17.

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.

18.
19.

BACE overexpression alters the subcellular processing of APP and inhibits Abeta deposition in vivo.

Lee EB, Zhang B, Liu K, Greenbaum EA, Doms RW, Trojanowski JQ, Lee VM.

J Cell Biol. 2005 Jan 17;168(2):291-302. Epub 2005 Jan 10.

20.

GEPT extract reduces Abeta deposition by regulating the balance between production and degradation of Abeta in APPV717I transgenic mice.

Tian J, Shi J, Zhang L, Yin J, Hu Q, Xu Y, Sheng S, Wang P, Ren Y, Wang R, Wang Y.

Curr Alzheimer Res. 2009 Apr;6(2):118-31.

PMID:
19355846
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