Small-molecule aggregation inhibitors reduce excess amyloid in a trisomy 16 mouse cortical cell line

Biological Research

Volumn 41, Issue 2, 2008, Pages 129-136

  Paula Lima, Andréa C ^a   Arriagada, Christian ^b   Toro, Rodrigo ^c   Cárdenas, Ana María ^c   Caviedes, Raúl ^b   Ferreira, Sergio T ^a   Caviedes, Pablo ^b  

^a FEDERAL UNIVERSITY OF RIO DE JANEIRO   (Brazil)

^b UNIVERSITY OF CHILE   (Chile)

^c UNIVERSIDAD DE VALPARAÍSO   (Chile)

Author keywords

Alzheimer's disease; Down syndrome; Intracellular amyloid; Murine trisomy 16; Small molecule inhibitors

Indexed keywords

2,4 DINITROPHENOL; 3 NITROPHENOL; 4 ACETANISIDINE; AMYLOID PRECURSOR PROTEIN; CALCIUM ION;

ANIMAL CELL; ARTICLE; BRAIN CORTEX; CALCIUM CELL LEVEL; CELL LINE; CONTROLLED STUDY; CYTOTOXICITY; DOWN SYNDROME; DRUG MECHANISM; MOUSE; NONHUMAN; PROTEIN AGGREGATION; PROTEIN EXPRESSION; TRISOMY 16;

2,4-DINITROPHENOL; ALZHEIMER DISEASE; AMYLOID BETA-PROTEIN PRECURSOR; ANILINE COMPOUNDS; ANIMALS; CELL LINE; CEREBRAL CORTEX; DISEASE MODELS, ANIMAL; DOWN SYNDROME; MICE; NITROPHENOLS;

ANIMALIA; MURINAE;

EID: 59849093117     PISSN: 07169760     EISSN: 07176287     Source Type: Journal    
DOI: None     Document Type: Article

References (35)

1. ALLEN DD, MARTIN J, ARRIAGADA C, CARDENAS AM, RAPOPORT SI, CAVIEDES R, CAVIEDES P (2000) Impaired cholinergic function in cell lines derived from the cerebral cortex of normal and trisomy 16 mice. Eur J Neurosci 12: 3259-3264
2. ALMEIDA CG, TAKAHASHI RH, GOURAS GK (2006) β-amyloid accumulation impairs multivesicular body sorting by inhibiting the ubiquitin-proteasome system. J Neurosci 26: 4277-4288
3. ARRIAGADA C, ASTORGA C, ATWATER I, ROJAS E, MEARS D, CAVIEDES R CAVIEDES (2007) Endosomal abnormalities related to amyloid precursor protein in cholesterol treated cerebral cortex neuronal cells derived from trisomy 16 mice, an animal model of Down syndrome. Neurosci Lett: 423 173-177
4. BEGNIA B, BRIGHINA L, FUMAGALLIA L, ANDREONIA S, CASTELLI E, FRANCESCONIC C, DEL BO R, BRESOLIN N, FERRARESE C (2003) Altered glutamate uptake in peripheral tissues from Down Syndrome patients. Neurosci Lett 343: 73-76
5. BUSCIGLIO J, PELSMAN A, WONG C, PIGINO G, YUAN M, MORI H, YANKNER BA (2002) Altered metabolism of the amyloid β precursor protein is associated with mitochondrial dysfunction in Down's syndrome. Neuron 33: 677-688
6. CÁRDENAS AM, RODRÍGUEZ MP, CORTÉS MP, ÁLVAREZ RM, WEI MP, RAPOPORT SI, SHIMAHARA T, CAVIEDES R, CAVIEDES P (1999) Calcium signals in cell lines derived from the cerebral cortex of normal and trisomy 16 mice. NeuroReport 10: 363-369
7. CATALDO AM, PETERHOFF CM, TRONCOSO JC, GOMEZ-ISLA T, HYMAN BT, NIXON RA (2000) Endocytic pathway abnormalities precede amyloid beta deposition in sporadic Alzheimer's disease and Down syndrome: differential effects of APOE genotype and presenilin mutations. Am J Pathol 157: 277-286
8. CATALDO AM, PETANCESKA S, PETERHOFF CM, TERIO NB, EPSTEIN CJ, VILLAR A, CARLSON EJ, STAUFENBIEL M, NIXON RA (2003) APP gene dosage modulates endosomal abnormalities of Alzheimer's disease in a segmental trisomy 16 mouse model of Down syndrome. J Neurosci 23: 6788-6792
9. DE FELICE FG, HOUZEL JC, GARCÍA-ABREU J, LENT R, LOUZADA PR Jr., AFONSO RC, MEIRELLES MN, NETO VM, FERREIRA ST (2001) Inhibition of Alzheimer's disease beta-amyloid aggregation, neurotoxicity, and in vivo deposition by nitrophenols: implications for Alzheimer's therapy. FASEB J 7: 1297-1299
10. DE FELICE FG, FERREIRA ST (2002) Beta-amyloid production, aggregation, and clearance as targets for therapy in Alzheimer's disease. Cell Mol Neurobiol 22: 545-563
11. DE FELICE FG, VIEIRA MN, SARAIVA LM, FIGUEROA-VILLAR JD, GARCIA-ABREU J., LIU R, CHANG L, KLEIN WL, FERREIRA ST (2004) Targeting the neurotoxic species in Alzheimer's disease: inhibitors of A? oligomerization. FASEB J 18: 1366-1372
12. ECHEVERRÍA V, CUELLO AC (2002) Intracellular Aβ amyloid, a sign for worse things to come? Mol Neurobiol 26: 299-316
13. FERREIRA ST, VIEIRA MN, DE FELICE FG (2007) Soluble protein oligomers as emerging toxins in Alzheimer's and other amyloid diseases. IUBMB Life.59(4-5):332-45.
14. GALDZICKI Z, SIAREY RJ (2003) Understanding mental retardation in Down's syndrome using trisomy 16 mouse models. Genes Brain Behav 2: 167-178
15. GELLER LN, POTTER H (1999) Chromosome missegregation and trisomy 21 mosaicism in Alzheimer's disease. Neurobiol Dis 6: 167-179
16. GLABE C (2001) Intracellular mechanisms of amyloid accumulation and pathogenesis in Alzheimer's disease. J Mol Neurosci 17: 137-145
17. GOURAS GK, TSAI J, NASLUND J, VINCENT B, EDGAR M, CHECLER F, GREENFIELD JP, HAROUTUNIAN V, BUXBAUM JD, XU H, GREENGARD P, RELKIN NR (2000) Intraneuronal Abeta42 accumulation in human brain. Am J Pathol 156: 15-20
18. GOURAS GK, ALMEIDA CG, TAKAHASHI RH (2005) Intraneuronal Abeta accumulation and origin of plaques in Alzheimer's disease. Neurobiol Aging 26: 1235-1244
19. GRALLE M, FERREIRA, ST (2007) Structure and functions of the human amyloid precursor protein: The whole is more than the sum of its parts. Progress in Neurobiology 82: 11-32
20. HAASS C, SELKOE DJ (2007) Soluble protein oligomers in neurodegeneration: lessons from the Alzheimer's amyloid beta-peptide. Nat Rev Mol Cell Biol 8: 101-112
21. HARDY J, SELKOE DJ (2002) The amyloid hypothesis of Alzheimer's disease: progress and problems on the road to therapeutics. Science 297: 353-356
22. KIENLEN-CAMPARD P, MIOLET S, TASIAUX B, OCTAVE JN (2002) Intracellular amyloid-beta 1-42, but not extracellular soluble amyloid-beta peptides, induces neuronal apoptosis. J Biol Chem 277: 15666-15670
23. LACOR PN, BUNIEL MC, FURLOW PW, CLEMENTE AS, VELASCO PT, WOOD M, VIOLA KL, KLEIN WL (2007) A oligomer-induced aberrations in synapse composition, shape, and density provide a molecular basis for loss of connectivity in Alzheimer's disease. J Neurosci 27: 796-807
24. LANGUI D, GIRARDOT N, EL HACHIMI KH, ALLINQUANT B, BLANCHARD V, PRADIER L, DUYCKAERTS C (2004) Subcellular topography of neuronal Abeta peptide in APPxPS1 transgenic mice. Am J Pathol 165: 1465-1477
25. LORENZO A, YANKNER BA (1994) Beta-amyloid neurotoxicity requires fibril formation and is inhibited by congo red. Proc Nat Acad Sc USA 91: 12243-12247
26. OPAZO P, SAUD K, DE SAINT PIERRE M, CÁRDENAS AM, ALLEN DD, SEGURA-AGUILAR J, CAVIEDES R, CAVIEDES P (2006) Knockdown of amyloid precursor protein normalizes cholinergic function in a cell line derived from the cerebral cortex of a trisomy 16 mouse: an animal model of Down Syndrome. J Neurosci Res 84:1303-1310
27. PIKE CJ, WALENCEWICZ-WASSERMAN AJ, KOSMOSKI J, CRIBBS DH, GLABE CG, COTMAN CW (1995) Structure-activity analyses of beta-amyloid peptides: contributions of the beta 25-35 region to aggregation and neurotoxicity. J Neurochem 64: 253-265
28. POLLARD HB, ARISPE N, ROJAS E (1995) Ion channel hypothesis for Alzheimer amyloid peptide neurotoxicity. Cell Mol Neurobiol 15: 513-526
29. PUCHTLER H, SWEAT F (1965) Congo red as a stain for fluorescence microscopy of amyloid. J Histochem Cytochem 13: 693-694
30. SAUD K, ARRIAGADA C, CÁRDENAS AM, SHIMAHARA T, ALLEN DD, CAVIEDES R, CAVIEDES P (2006) Neuronal dysfunction in Down syndrome: Contribution of neuronal models in cell culture. J Physiol Paris 99: 201-210
31. SELKOE DJ (1991) The molecular pathology of Alzheimer's disease. Neuron 6: 487-498
32. TAKAHASHI RH, MILNER TA, LI F, NAME E, EDGAR MA, YAMAGUCHI H, BEAL MF, XU H, GREENGARD P, GOURAS GK (2002) Intraneuronal Alzheimer Abeta42 accumulates in multivesicular bodies and is associated with synaptic pathology. Am J Pathol 161: 1869-1879
33. VIEIRA MN, FIGUEROA-VILLAR JD, MEIRELLES MN, FERREIRA ST, DE FELICE FG (2006) Small molecule inhibitors of lysozyme amyloid aggregation. Cell Biochem Biophys 44: 549-553
34. WASILEWSKA-SAMPAIO AP, SILVEIRA MS, HOLUB O, GOECKING R, GOMES FC, NETO VM, LINDEN R, FERREIRA ST, DE FELICE FG (2005) Neuritogenesis and neuronal differentiation promoted by 2,4-dinitrophenol, a novel anti-amyloidogenic compound. FASEB J 19: 1627-1636
35. WIRTHS O, MULTHAUP G, CZECH C, BLANCHARD V, MOUSSAOUI S, TREMP G, PRADIER L, BEYREUTHER K, BAYER TA (2001) Intraneuronal Abeta accumulation precedes plaque formation in beta-amyloid precursor protein and presenilin-1 double-transgenic mice. Neurosci Lett 306: 116-120