Oligomerization and neurotoxicity of the amyloid ADan peptide implicated in familial Danish dementia

Journal of Neurochemistry

Volumn 88, Issue 2, 2004, Pages 281-290

  Gibson, Gillian ^a   Gunasekera, Nicola ^a   Lee, Maria ^a   Lelyveld, Victor ^a   El Agnaf, Omar M A ^a,c   Wright, Andrew ^b   Austen, Brian ^a  

^a ST GEORGE'S UNIVERSITY OF LONDON   (United Kingdom)

^b GLYNDWR UNIVERSITY   (United Kingdom)

^c LANCASTER UNIVERSITY   (United Kingdom)

Author keywords

ADan; Amyloid; BRI; Danish dementia; Neurotoxicity; Oligomers

Indexed keywords

AMYLOID ADAN PEPTIDE; AMYLOID PROTEIN; OLIGOMER; UNCLASSIFIED DRUG;

ARTICLE; ATOMIC FORCE MICROSCOPY; ATOMIC FORCE SPECTROSCOPY; BRI GENE; CELL LINE; CENTRAL NERVOUS SYSTEM; CLINICAL FEATURE; CODON; CONTROLLED STUDY; DEGENERATIVE DISEASE; DEMENTIA; DENMARK; ELECTRON MICROSCOPY; FAMILIAL DANISH DEMENTIA; FAMILIAL DISEASE; GENE; GENE MUTATION; HUMAN; HUMAN CELL; IN VITRO STUDY; NERVE CELL CULTURE; NEUROFIBRILLARY DEGENERATION; NEUROFIBRILLARY TANGLE; NEUROTOXICITY; OLIGOMERIZATION; PATHOGENESIS; PRIORITY JOURNAL; PROTEIN AGGREGATION; PROTEIN LOCALIZATION; SPECTROSCOPY; VASCULAR AMYLOIDOSIS;

DAUCUS CAROTA;

EID: 0347087364     PISSN: 00223042     EISSN: None     Source Type: Journal    
DOI: 10.1046/j.1471-4159.2003.02134.x     Document Type: Article

References (23)

1. Aikawa H., Suzuki K., Iwasaki Y. and Iiuzuka R. (1985) Atypical Alzheimer's disease with spastic paresis and ataxia. Ann. Neurol. 17, 297-300.
2. Bieschke J., Giese A., Schulz-Schaeffer W., Zerr I., Poser S., Eigen M. and Kretzschmar H. (2000) Ultrasensitive detection of pathological prion protein aggregates by dual-color scanning for intensely fluorescent targets. Proc. Natl Acad. Sci. USA 97, 5468-5473.
3. Bucciantini M., Giannoni E., Chiti F. et al. (2002) Inherent toxicity of aggregates implies a common mechanism for protein misfolding diseases. Nature 416, 507-511.
4. Chiesa R., Piccardo P., Ghetti B. and Harris D. A. (1998) Neurological illness in transgenic mice expressing a prion protein with an insertional mutation. Neuron 6, 1339-1351.
5. Conway K. A., Lee S. J., Rochet J. C., Ding T. T., Williamson R. E. and Lansbury P. T. Jr (2000) Acceleration of oligomerization, not fibrillization, is a shared property of both α-synuclein mutations linked to early-onset Parkinson's disease: implications for pathogenesis and therapy. Proc. Natl Acad. Sci. USA 97, 571-576.
6. El-Agnaf O. M. A., Jakes R., Curran M. D., Middletone D., Ingenito F., Bianchi E., Pessi A., Neill D. and Wallace A. (1998) Aggregates from mutant and wild-type α-synuclein proteins and NAC peptide induce apoptotic cell death in human neuroblastoma cells by formation of β-sheet and amyloid-like filaments. FEBS Lett. 440, 71-75.
7. El-Agnaf O. M. A., Mahil D. S., Patel B. P. and Austen B. A. (2000) Oligomerization and toxicity of β-amyloid-42 implicated in Alzheimer's disease. Biochem. Biophy. Res. Commun. 237, 1003-1007.
8. El-Agnaf O. M., Nagala S., Patel B. P. and Austen B. M. (2001a) Non-fibrillar oligomeric species of the amyloid ABri peptide, implicated in familial British dementia, are more potent at inducing apoptotic cell death than protofibrils or mature fibrils. J. Mol. Biol. 310, 157-168.
9. El-Agnaf O. M. A., Sheridan J. M., Sidera C., Siligardi G., Hussain R., Haris P. I. and Austen B. M. (2001b) Effect of the disulphide bridge and the C-terminal extension on the oligomerisation of the amyloid peptide ABri implicated in familial British dementia. Biochemistry 40, 3449-3457.
10. Giese A., Bieschke J., Eigen M. and Kretzschmar H. A. (2000) Putting prions into focus: application of single molecule detection to the diagnosis of prion diseases. Arch. Virol. Suppl. 16, 161-171.
11. Goldberg M. S. and Lansbury P. T. (2000) Is there a cause-and-effect relationship between α-synuclein fibrillization and Parkinson's disease? Nat. Cell Biol. 2, 115-119.
12. Holton J. L., Lashley T., Ghiso J. et al. (2002) Familial Danish dementia: a novel form of cerebral amyloidosis associated with deposition of both amyloid-Dan and amyloid-β. J. Neuropathol. Exp. Neurol. 61, 254-267.
13. Lambert M. P., Barlow A. K., Chromy B. A. et al. (1998) Diffusible, nonfibrillar ligands derived from Aβ1-42 are potent central nervous system neurotoxins. Proc. Natl Acad. Sci. USA 95, 6448-6453.
14. Masliah E., Rockenstein E., Veinbergs I., Mallory M., Hashimoto M., Takeda A., Sagara Y., Sisk A. and Mucke L. (2000) Dopaminergic loss and inclusion body formation in α-synuclein mice: implications for neurodegenerative disorders. Science 287, 1265-1269.
15. Pitschke M., Prior R., Haupt M. and Riesner D. (1998) Detection of single amyloid β-protein aggregates in the cerebrospinal fluid of Alzheimer's patients by fluorescence correlation spectroscopy. Nat. Med. 4, 832-834.
16. Plant G. T., Revesz T., Barnard R. O., Harding A. E. and Gautier-Smith P. C. (1990) Familial cerebral amyloid angiopathy with nonneuritic amyloid plaque formation. Brain 13, 721-747.
17. Saudou F., Finkbeiner S., Devys D. and Greenberg M. E. (1998) Huntingtin acts in the nucleus to induce apoptosis but death does not correlate with the formation of intranuclear inclusions. Cell 95, 55-66.
18. Sian A. K., Frears E. R., El-Agnaf O. M. A., Patel B. P., Manca M. F., Siligardi G., Hussain R. and Austen B. A. (2000) Oligomerization of β-amyloid of the Alzheimer's and Dutch cerebral haemorrage types. Biochem. J. 349, 299-308.
19. Van der Putten H., Wiederhold K. H., Probst A. et al. (2000) Neuropathology in mice expressing human α-synuclein. J. Neurosci. 20, 6021-6029.
20. Vidal R., Frangione B., Rostagno A., Mead S., Revesz T., Plant G. and Ghiso J. (1999) A stop-codon mutation in the BRI gene associated with familial British dementia. Nature 399, 776-781.
21. Vidal R., Revesz T., Rostagno A., Kim E. et al. (2000) A decamer duplication in the 3′ region of the BRI gene originates an amyloid peptide that is associated with dementia in a Danish kindred. Proc. Natl Acad. Sci. USA 97, 4920-4925.
22. Walsh D. M., Klyubin I., Fadeeva J. V., Cullen W. K., Anwyl R., Wolfe M. S., Rowan M. J. and Selkoe D. J. (2002) Naturally secreted oligomers of amyloid β protein potently inhibit hippocampal long-term potentiation in vivo. Nature 416, 535-539.
23. Worster-Drought C., Hill T. R. and McMenemey W. H. (1933) Familial cerebral amyloid angiopathy with non-neuritic plaque formation. J. Neurol. Psychopathol. 14, 27-34.