Amyloid β neurotoxicity in the cholinergic but not in the serotonergic phenotype of RN46A cells

Molecular Brain Research

Volumn 57, Issue 2, 1998, Pages 266-274

  Olesen, Ole F ^a   Dagø, Lone ^a   Mikkelsen, Jens D ^a  

^a H LUNDBECK A S   (Denmark)

Author keywords

Alzheimer's disease; Amyloid peptide; Cellular redox activity; Cholinergic; Serotonergic

Indexed keywords

AMYLOID BETA PROTEIN; BRAIN DERIVED NEUROTROPHIC FACTOR;

ANIMAL CELL; ARTICLE; CELL DIFFERENTIATION; CELL STRAIN; CHO CELL; CHOLINERGIC NERVE CELL; NEUROCHEMISTRY; NEUROTOXICITY; NONHUMAN; PRIORITY JOURNAL; RAPHE NUCLEUS;

ACETYLCHOLINE; AMYLOID BETA-PROTEIN; ANIMALS; ANTIGENS, POLYOMAVIRUS TRANSFORMING; CELLS, CULTURED; CHO CELLS; CRICETINAE; FEMALE; GESTATIONAL AGE; NEURONS; NEUROTOXINS; PC12 CELLS; PHENOTYPE; PREGNANCY; RAPHE NUCLEI; RATS; RATS, WISTAR; RETROVIRIDAE; SEROTONIN;

ANIMALIA;

EID: 0032525799     PISSN: 0169328X     EISSN: None     Source Type: Journal    
DOI: 10.1016/S0169-328X(98)00096-5     Document Type: Article

References (40)

1. Abe E., Casamenti F., Giovannelli L., Scali C., Pepeu G. Administration of amyloid β-peptides into the medial septum of rats decreases acetylcholine release from hippocampus in vivo. Brain Res. 636:1994;162-164.
2. 1-antichymotrypsin in the brain amyloid deposits of Alzheimer's disease. Cell. 52:1988;487-501.
3. Behl C., Davis J., Cole G.M., Schubert D. Vitamin E protects nerve cells from amyloid β protein toxicity. Biochem. Biophys. Res. Commun. 186:1992;944-950.
4. Behl C., Schubert D. Heat shock partially protects rat pheochromocytoma PC12 cells from amyloid β peptide toxicity. Neurosci. Lett. 154:1993;1-4.
5. 1-40 ratio in vitro and in vivo. Neuron. 17:1996;1005-1013.
6. Cai X.D., Golde T.E., Younkin S.G. Release of excess amyloid β protein from a mutant amyloid β protein precursor. Science. 259:1993;514-516.
7. Chartier-Harlin M.C., Crawford F., Houlden H., Warren A., Hughes D., Fidani L., Goate A., Rossor M., Roques P., Hardy J., Mullan M. Early-onset Alzheimer's disease caused by mutations at codon 717 of the β-amyloid precursor protein gene. Nature. 353:1991;844-846.
8. Citron M., Oltersdorf T., Haass C., McConlogue L., Hung A.Y., Seubert P., Vigo-Pelfrey C., Lieberburg I., Selkoe D.J. Mutation of the β-amyloid precursor protein in familial Alzheimer's disease increases β-protein production. Nature. 360:1992;672-674.
9. Citron M., Westaway D., Xia W., Carlson G., Diehl T., Levesque G., Johnson-Wood K., Lee M., Seubert P., Davis A. Mutant presenilins of Alzheimer's disease increase production of 42-residue amyloid β-protein in both transfected cells and transgenic mice. Nature Med. 3:1997;67-72.
10. El Khoury J., Hickman S.E., Thomas C.A., Cao L., Silverstein S.C., Loike J.D. Scavenger receptor-mediated adhesion of microglia to β- amyloid fibrils. Nature. 382:1996;716-719.
11. Goate A., Chartier-Harlin M.C., Mullan M., Brown J., Crawford F., Fidani L., Giuffra L., Haynes A., Irving N., James L., Mant R., Newton P., Roques P., Talbot C., Pericak-Vance M., Roses A., Williamson R., Rossor M., Owen M., Hardy J. Segregation of a missense mutation in the amyloid precursor protein gene with familial Alzheimer's disease. Nature. 349:1991;704-706.
12. Gschwind M., Huber G. Apoptotic cell death induced by β-amyloid 1-42 peptide is cell type dependent. J. Neurochem. 65:1995;292-300.
13. Haass C., Schlossmacher M.G., Hung A.Y., Vigo-Pelfrey C., Mellon A., Ostaszewski B.L., Lieberburg I., Koo E.H., Schenk D., Teplow D.B. Amyloid β-peptide is produced by cultured cells during normal metabolism. Nature. 359:1992;322-325.
14. Harkany T., De Jong G.I., Soos K., Penke B., Luiten P.G., Gulya K. β-amyloid (1-42) affects cholinergic but not parvalbumin- containing neurons in the septal complex of the rat. Brain Res. 698:1995;270-274.
15. Jarrett J.T., Berger E.P., Lansbury P.T. Jr. The carboxy terminus of the β amyloid protein is critical for the seeding of amyloid formation: implications for the pathogenesis of Alzheimer's disease. Biochemistry. 32:1993;4693-4697.
16. Knauer M.F., Soreghan B., Burdick D., Kosmoski J., Glabe C.G. Intracellular accumulation and resistance to degradation of the Alzheimer amyloid A4/β protein. Proc. Natl. Acad. Sci. USA. 89:1992;7437-7441.
17. Koh J.Y., Yang L.L., Cotman C.W. β-amyloid protein increases the vulnerability of cultured cortical neurons to excitotoxic damage. Brain Res. 533:1990;315-320.
18. Liu Y., Schubert D. Cytotoxic amyloid peptides inhibit cellular 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyltetrazolium bromide (MTT) reduction by enhancing MTT formazan exocytosis. J. Neurochem. 69:1997;2285-2293.
19. Mamounas L.A., Blue M.E., Siuciak J.A., Altar C.A. Brain-derived neurotrophic factor promotes the survival and sprouting of serotonergic axons in rat brain. J. Neurosci. 15:1995;7929-7939.
20. Mattson M.P., Cheng B., Davis D., Bryant K., Lieberburg I., Rydel R.E. β-Amyloid peptides destabilize calcium homeostasis and render human cortical neurons vulnerable to excitotoxicity. J. Neurosci. 12:1992;376-389.
21. Murrell J., Farlow M., Ghetti B., Benson M.D. A mutation in the amyloid precursor protein associated with hereditary Alzheimer's disease. Science. 254:1991;97-99.
22. Namba Y., Tomonaga M., Kawasaki H., Otomo E., Ikeda K. Apolipoprotein E immunoreactivity in cerebral amyloid deposits and neurofibrillary tangles in Alzheimer's disease and kuru plaque amyloid in Creutzfeldt-Jakob disease. Brain Res. 541:1991;163-166.
23. Narisawa-Saito M., Wakabayashi K., Tsuji S., Takahashi H., Nawa H. Regional specificity of alterations in NGF, BDNF and NT-3 levels in Alzheimer's disease. NeuroReport. 7:1996;2925-2928.
24. Phillips H.S., Hains J.M., Armanini M., Laramee G.R., Johnson S.A., Winslow J.W. BDNF mRNA is decreased in the hippocampus of individuals with Alzheimer's disease. Neuron. 7:1991;695-702.
25. Pike C.J., Burdick D., Walencewicz A.J., Glabe C.G., Cotman C.W. Neurodegeneration induced by β-amyloid peptides in vitro: the role of peptide assembly state. J. Neurosci. 13:1993;1676-1687.
26. Pike C.J., Cotman C.W. Cultured GABA-immunoreactive neurons are resistant to toxicity induced by β-amyloid. Neuroscience. 56:1993;269-274.
27. Pollack S.J., Sadler I.I., Hawtin S.R., Tailor V.J., Shearman M.S. Sulfated glycosaminoglycans and dyes attenuate the neurotoxic effects of β-amyloid in rat PC12 cells. Neurosci. Lett. 184:1995;113-116.
28. Rudge J.S., Eaton M.J., Mather P., Lindsay R.M., Whittemore S.R. CNTF induces raphe neuronal precursors to switch from a serotonergic to a cholinergic phenotype in vitro. Mol. Cell Neurosci. 7:1996;204-221.
29. Scheuner D., Eckman C., Jensen M., Song X., Citron M., Suzuki N., Bird T.D., Hardy J., Hutton M., Kukull W., Larson E., Levy-Lahad E., Viitanen M., Peskind E., Poorkaj P., Schellenberg G., Tanzi R., Wasco W., Lannfelt L., Selkoe D., Younkin S. Secreted amyloid β-protein similar to that in the senile plaques of Alzheimer's disease is increased in vivo by the presenilin 1 and 2 and APP mutations linked to familial Alzheimer's disease. Nat. Med. 2:1996;864-870.
30. Segal R.A., Greenberg M.E. Intracellular signaling pathways activated by neurotrophic factors. Annu. Rev. Neurosci. 19:1996;463-489.
31. Shearman M.S., Ragan C.I., Iversen L.L. Inhibition of PC12 cell redox activity is a specific, early indicator of the mechanism of β-amyloid-mediated cell death. Proc. Natl. Acad. Sci. USA. 91:1994;1470-1474.
32. Shoji M., Golde T.E., Ghiso J., Cheung T.T., Estus S., Shaffer L.M., Cai X.D., McKay D.M., Tintner R., Frangione B. Production of the Alzheimer amyloid β protein by normal proteolytic processing. Science. 258:1992;126-129.
33. Snow A.D., Mar H., Nochlin D., Kimata K., Kato M., Suzuki S., Hassell J., Wight T.N. The presence of heparan sulfate proteoglycans in the neuritic plaques and congophilic angiopathy in Alzheimer's disease. Am. J. Pathol. 133:1988;456-463.
34. Storandt M., Hill R.D. Very mild senile dementia of the Alzheimer type: II. Psychometric test performance. Arch. Neurol. 46:1989;383-386.
35. Tomita T., Maruyama K., Saido T.C., Kume H., Shinozaki K., Tokuhiro S., Capell A., Walter J., Gruenberg H., Haass C. The presenilin 2 mutation (N141l) linked to familial Alzheimer disease (Volga German families) increase the secretion of amyloid β protein ending at the 42nd (or 43rd) residue. Proc. Natl. Acad. Sci. USA. 94:1997;2025-2030.
36. Ueda K., Fukushima H., Masliah E., Xia Y., Iwai A., Yoshimoto M., Otero D.A., Kondo J., Ihara Y., Saitoh T. Molecular cloning of cDNA encoding an unrecognized component of amyloid in Alzheimer disease. Proc. Natl. Acad. Sci. USA. 90:1993;11282-11286.
37. White L.A., Eaton M.J., Castro M.C., Klose K.J., Globus M.Y., Shaw G., Whittemore S.R. Distinct regulatory pathways control neurofilament expression and neurotransmitter synthesis in immortalized serotonergic neurons. J. Neurosci. 14:1994;6744-6753.
38. Yan S.D., Chen X., Fu J., Chen M., Zhu H., Roher A., Slattery T., Zhao L., Nagashima M., Morser J., Migheli A., Nawroth P., Stern D., Schmidt A.M. RAGE and amyloid-β peptide neurotoxicity in Alzheimer's disease. Nature. 382:1996;685-691.
39. Yan S.D., Fu J., Soto C., Chen X., Zhu H., Al-Mohanna F., Collison K., Zhu A., Stern E., Saido T., Tohyama M., Ogawa S., Roher A., Stern D. An intracellular protein that binds amyloid-β peptide and mediates neurotoxicity in Alzheimer's disease. Nature. 389:1997;689-695.
40. Yankner B.A., Duffy L.K., Kirschner D.A. Neurotrophic and neurotoxic effects of amyloid β protein: reversal by tachykinin neuropeptides. Science. 250:1990;279-282.