CoChat
Sign Up
Cited by 55

The DOI matches its Crossref record; 4 of the 4 references it cites were found in a registry or an index.

A Drosophila Model of Alzheimer's Disease

Crowther, Damian C., Page, Richard, Chandraratna, Dhianjali, Lomas, David A.·2006·Methods in Enzymology
DOI 10.1016/s0076-6879(06)12015-7
Open this paper in CoChat — free account

Abstract

The development of a model of Alzheimer's disease in Drosophila allows us to identify and dissect pathological pathways using the most powerful genetic tools available to biology. By reconstructing essential steps in Alzheimer's pathology, such as amyloid beta peptide and tau overexpression, we can observe clear and rapid phenotypes that are surrogate markers for human disease. The characterization of progressive phenotypes by immunohistochemistry of the brain combined with longevity, climbing, and pseudopupil assays allows the investigator to generate quantitative data. Phenotypes may be modulated by changes in gene expression as part of a genetic screen or by potential therapeutic compounds.

Overview

Integrity signals

Registry

Crossref · 10.1016/s0076-6879(06)12015-7

Cites

4 of 4 references verified0 citation errors · 0 not checkable

Statistics

Recomputing p-values needs the paper’s full text.

Verification

Claims the paper makes

This paper’s full text isn’t openly available, so its claims and self-check weren’t run. The registry and citation checks still apply.

Claims other papers make about this one

Each is checked against this paper’s own text: does it say what the citing paper says it does?

Citations

Cites

Flagged first, then by citations

Research works printed but not linked: 48

  1. Aigaki, 2001, The gene search system: Its application to functional genomics in Drosophila melanogaster, J. Neurogenet., 15, 169, 10.3109/01677060109167374 · DOI
  2. Bellen, 2004, The BDGP gene disruption project: Single transposon insertions associated with 40% of Drosophila genes, Genetics, 167, 761, 10.1534/genetics.104.026427 · DOI
  3. Berger, 2001, Genetic mapping with SNP markers in Drosophila, Nat. Genet., 29, 475, 10.1038/ng773 · DOI
  4. Brand, 1993, Targeted gene expression as a means of altering cell fates and generating dominant phenotypes, Development, 118, 401, 10.1242/dev.118.2.401 · DOI
  5. Chyung, 1997, Novel beta‐secretase cleavage of beta‐amyloid precursor protein in the endoplasmic reticulum/intermediate compartment of NT2N cells, J. Cell. Biol., 138, 671, 10.1083/jcb.138.3.671 · DOI
  6. Chyung, 2005, Gamma‐secretase exists on the plasma membrane as an intact complex that accepts substrates and effects intramembrane cleavage, J. Biol. Chem., 280, 4383, 10.1074/jbc.M409272200 · DOI
  7. Cook, 1997, Alzheimer's A beta(1‐42) is generated in the endoplasmic reticulum/intermediate compartment of NT2N cells, Nat. Med., 3, 1021, 10.1038/nm0997-1021 · DOI
  8. Crowther, 2002, Familial conformational diseases and dementias, Hum. Mutat., 20, 1, 10.1002/humu.10100 · DOI
  9. Crowther, 2005, Intraneuronal Ab, non‐amyloid aggregates and neurodegeneration in a Drosophila model of Alzheimer's disease, Neuroscience, 132, 123, 10.1016/j.neuroscience.2004.12.025 · DOI
  10. Dickson, 1997, The pathogenesis of senile plaques, J. Neuropathol. Exp. Neurol., 56, 321, 10.1097/00005072-199704000-00001 · DOI · Paper page
  11. Doerflinger, 2003, The role of PAR‐1 in regulating the polarised microtubule cytoskeleton in the Drosophila follicular epithelium, Development, 130, 3965, 10.1242/dev.00616 · DOI
  12. Finelli, 2004, A model for studying Alzheimer's Abeta42‐induced toxicity in Drosophila melanogaster, Mol. Cell Neurosci., 26, 365, 10.1016/j.mcn.2004.03.001 · DOI
  13. Fossgreen, 1998, Transgenic Drosophila expressing human amyloid precursor protein show g‐secretase activity and blistered wing phenotype, Proc. Natl. Acad. Sci. USA, 95, 13703, 10.1073/pnas.95.23.13703 · DOI
  14. German, 2004, Mouse models of Alzheimer's disease: Insight into treatment, Rev. Neurosci., 15, 353, 10.1515/REVNEURO.2004.15.5.353 · DOI
  15. Glenner, 1984, Alzheimer's disease and Down's syndrome: Sharing of a unique cerebrovascular amyloid fibril protein, Biochem. Biophys. Res. Commun., 122, 1131, 10.1016/0006-291X(84)91209-9 · DOI · Paper page
  16. Glenner, 1984, Alzheimer's disease: Initial report of the purification and characterization of a novel cerebrovascular amyloid protein, Biochem. Biophys. Res. Commun., 120, 885, 10.1016/S0006-291X(84)80190-4 · DOI · Paper page
  17. Goedert, 1988, Cloning and sequencing of the cDNA encoding a core protein of the paired helical filament of Alzheimer disease: Identification as the microtubule‐associated protein tau, Proc. Natl. Acad. Sci. USA, 85, 4051, 10.1073/pnas.85.11.4051 · DOI · Paper page
  18. Greeve, 2004, Age‐dependent neurodegeneration and Alzheimer‐amyloid plaque formation in transgenic Drosophila, J. Neurosci., 24, 3899, 10.1523/JNEUROSCI.0283-04.2004 · DOI
  19. Hoyert, 2005, Deaths: Preliminary data for 2003, Natl. Vital Stat. Rep., 53, 1
  20. Iijima, 2004, Dissecting the pathological effects of human A{beta}40 and A{beta}42 in Drosophila: A potential model for Alzheimer's disease, Proc. Natl. Acad. Sci. USA, 101, 6623, 10.1073/pnas.0400895101 · DOI · Paper page
  21. Jackson, 1998, Polyglutamine‐expanded human huntingtin transgenes induce degeneration of Drosophila photoreceptor neurons, Neuron, 21, 633, 10.1016/S0896-6273(00)80573-5 · DOI
  22. Kayed, 2003, Common structure of soluble amyloid oligomers implies common mechanism of pathogenesis, Science, 300, 486, 10.1126/science.1079469 · DOI · Paper page
  23. Koo, 1994, Evidence that production and release of amyloid beta‐protein involves the endocytic pathway, J. Biol. Chem., 269, 17386, 10.1016/S0021-9258(17)32449-3 · DOI · Paper page
  24. Koundakjian, 2004, The Zuker collection: A resource for the analysis of autosomal gene function in Drosophila melanogaster, Genetics, 167, 203, 10.1534/genetics.167.1.203 · DOI
  25. Lambert, 1998, Diffusible, nonfibrillar ligands derived from Abeta1‐42 are potent central nervous system neurotoxins, Proc. Natl. Acad. Sci. USA, 95, 6448, 10.1073/pnas.95.11.6448 · DOI · Paper page
  26. Link, 2005, Invertebrate models of Alzheimer's disease, Genes Brain Behav., 4, 147, 10.1111/j.1601-183X.2004.00105.x · DOI
  27. Mata, 2000, Tribbles coordinates mitosis and morphogenesis in Drosophila by regulating string/CDC25 proteolysis, Cell, 101, 511, 10.1016/S0092-8674(00)80861-2 · DOI
  28. Parks, 2004, Systematic generation of high‐resolution deletion coverage of the Drosophila melanogaster genome, Nat. Genet., 36, 288, 10.1038/ng1312 · DOI
  29. Price, 1998, Alzheimer's disease: Genetic studies and transgenic models, Annu. Rev. Genet., 32, 461, 10.1146/annurev.genet.32.1.461 · DOI · Paper page
  30. Refolo, 1995, Evidence that secretase cleavage of cell surface Alzheimer amyloid precursor occurs after normal endocytic internalization, J. Neurosci. Res., 40, 694, 10.1002/jnr.490400515 · DOI
  31. Reichhart, 2002, Splice‐activated UAS hairpin vector gives complete RNAi knockout of single or double target transcripts in Drosophila melanogaster, Genesis, 34, 160, 10.1002/gene.10122 · DOI
  32. Rorth, 1996, A modular misexpression screen in Drosophila detecting tissue‐specific phenotypes, Proc. Natl. Acad. Sci. USA, 93, 12418, 10.1073/pnas.93.22.12418 · DOI
  33. Rubin, 1982, Genetic transformation of Drosophila with transposable element vectors, Science, 218, 348, 10.1126/science.6289436 · DOI
  34. Ryder, 2004, The DrosDel collection: A set of P‐element insertions for generating custom chromosomal aberrations in Drosophila melanogaster, Genetics, 167, 797, 10.1534/genetics.104.026658 · DOI
  35. Selkoe, 2000, Toward a comprehensive theory for Alzheimer's disease. Hypothesis: Alzheimer's disease is caused by the cerebral accumulation and cytotoxicity of amyloid beta‐protein, Ann. N. Y. Acad. Sci., 924, 17, 10.1111/j.1749-6632.2000.tb05554.x · DOI
  36. Shulman, 2003, Genetic modifiers of tauopathy in Drosophila, Genetics, 165, 1233, 10.1093/genetics/165.3.1233 · DOI · Paper page
  37. Spradling, 1982, Transposition of cloned P elements into Drosophila germ line chromosomes, Science, 218, 341, 10.1126/science.6289435 · DOI
  38. Struhl, 1999, Presenilin is required for activity and nuclear access of Notch in Drosophila, Nature, 398, 522, 10.1038/19091 · DOI
  39. Thinakaran, 1996, Metabolism of the “Swedish” amyloid precursor protein variant in neuro2a (N2a) cells. Evidence that cleavage at the “beta‐secretase” site occurs in the Golgi apparatus, J. Biol. Chem., 271, 9390, 10.1074/jbc.271.16.9390 · DOI · Paper page
  40. Toba, 1999, The gene search system. A method for efficient detection and rapid molecular identification of genes in Drosophila melanogaster, Genetics, 151, 725, 10.1093/genetics/151.2.725 · DOI
  41. Tully, 1985, Classical conditioning and retention in normal and mutant Drosophila melanogaster, J. Comp. Physiol. [A], 157, 263, 10.1007/BF01350033 · DOI
  42. Walsh, 2002, Naturally secreted oligomers of amyloid beta protein potently inhibit hippocampal long‐term potentiation in vivo, Nature, 416, 535, 10.1038/416535a · DOI · Paper page
  43. Wilcock, 1982, Plaques, tangles and dementia. A quantitative study, J. Neurol. Sci., 56, 343, 10.1016/0022-510X(82)90155-1 · DOI · Paper page
  44. Wild‐Bode, 1997, Intracellular generation and accumulation of amyloid beta‐peptide terminating at amino acid 42, J. Biol. Chem., 272, 16085, 10.1074/jbc.272.26.16085 · DOI · Paper page
  45. Williams, 2000, Tau and tau reporters disrupt central projections of sensory neurons in Drosophila, J. Comp. Neurol., 428, 630, 10.1002/1096-9861(20001225)428:4<630::AID-CNE4>3.0.CO;2-X · DOI · Paper page
  46. Wittmann, 2001, Tauopathy in Drosophila: Neurodegeneration without neurofibrillary tangles, Science, 293, 711, 10.1126/science.1062382 · DOI · Paper page
  47. Xu, 1997, Generation of Alzheimer beta‐amyloid protein in the trans‐Golgi network in the apparent absence of vesicle formation, Proc. Natl. Acad. Sci. USA, 94, 3748, 10.1073/pnas.94.8.3748 · DOI
  48. Ye, 1999, Neurogenic phenotypes and altered Notch processing in Drosophila presenilin mutants, Nature, 398, 525, 10.1038/19096 · DOI

Cited by

Sorted by citations

Metadata

Authors
Crowther, D. C., Page, R., Chandraratna, D., & Lomas, D. A.
Venue
Methods in Enzymology
Publisher
Elsevier
Published
2006
Pages
234-255
ISSN
0076-6879
DOI
10.1016/s0076-6879(06)12015-7
Cited by
55
References
4
Language
en

About these checks

Registry, retraction, Cites and statistics results are computed, not judged, with one exception: a printed reference that no index lists is read once by a model before it counts as a citation error. Claims are extracted by a model and kept only when their quote appears verbatim in the text; each cited source is then checked, with a model’s help, for whether it says what the claim relies on. Those verdicts can be wrong — read the claim’s quote and the cited source before relying on one.

Statistics and arithmetic are recomputed, not judged.

Confidence bands are shown only for fields calibrated on our annotated test set. None is calibrated yet, so no band is shown.

What counts as a claim ›How we measure confidence ›How we check this ›

Are you an author, or do you see a problem with this page? Request a review