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The DOI matches its Crossref record; 11 of the 11 references it cites were found in a registry or an index.

The Synaptic Accumulation of Hyperphosphorylated Tau Oligomers in Alzheimer Disease Is Associated With Dysfunction of the Ubiquitin-Proteasome System

Tai, Hwan-Ching, Serrano-Pozo, Alberto, Hashimoto, Tadafumi, Frosch, Matthew P., Spires-Jones, Tara L., Hyman, Bradley T.·2012·The American Journal of Pathology
DOI 10.1016/j.ajpath.2012.06.033
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  • During progression of AD and other tauopathies, abnormally phosphorylated forms of Tau aggregate and accumulate in the somatodendritic compartment in neurons and can localize to synapses.

    “During progression of AD and other tauopathies, abnormally phosphorylated forms of Tau aggregate and accumulate in the somatodendritic compartment in neurons and can localize to synapses (Ittner and Götz, 2011; Tai et al., 2012”

    From Changes in the Synaptic Proteome in Tauopathy and Rescue of Tau-Induced Synapse Loss by C1q Antibodies (2018) · cites this paper as Tai et al., 2012

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Research works printed but not linked: 36

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  4. Arriagada, 1992, Distribution of Alzheimer-type pathologic changes in nondemented elderly individuals matches the pattern in Alzheimer's disease, Neurology, 42, 1681, 10.1212/WNL.42.9.1681 · DOI · Paper page
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  7. Spires-Jones, 2009, Tau pathophysiology in neurodegeneration: a tangled issue, Trends Neurosci, 32, 150, 10.1016/j.tins.2008.11.007 · DOI
  8. Dotti, 1987, The expression and distribution of the microtubule-associated proteins tau and microtubule-associated protein 2 in hippocampal neurons in the rat in situ and in cell culture, Neuroscience, 23, 121, 10.1016/0306-4522(87)90276-4 · DOI
  9. Avila, 2004, Role of tau protein in both physiological and pathological conditions, Physiol Rev, 84, 361, 10.1152/physrev.00024.2003 · DOI · Paper page
  10. Brandt, 2005, Tau alteration and neuronal degeneration in tauopathies: mechanisms and models, Biochim Biophys Acta, 1739, 331, 10.1016/j.bbadis.2004.06.018 · DOI
  11. Ittner, 2010, Dendritic function of tau mediates amyloid-beta toxicity in Alzheimer's disease mouse models, Cell, 142, 387, 10.1016/j.cell.2010.06.036 · DOI · Paper page
  12. Cripps, 2006, Alzheimer disease-specific conformation of hyperphosphorylated paired helical filament-Tau is polyubiquitinated through Lys-48, Lys-11, and Lys-6 ubiquitin conjugation, J Biol Chem, 281, 10825, 10.1074/jbc.M512786200 · DOI · Paper page
  13. Yi, 2007, Emerging roles for ubiquitin and protein degradation in neuronal function, Pharmacol Rev, 59, 14, 10.1124/pr.59.1.4 · DOI · Paper page
  14. Keck, 2003, Proteasome inhibition by paired helical filament-tau in brains of patients with Alzheimer's disease, J Neurochem, 85, 115, 10.1046/j.1471-4159.2003.01642.x · DOI · Paper page
  15. Hollingsworth, 1985, Biochemical characterization of a filtered synaptoneurosome preparation from guinea pig cerebral cortex: cyclic adenosine 3′:5′-monophosphate-generating systems, receptors, and enzymes, J Neurosci, 5, 2240, 10.1523/JNEUROSCI.05-08-02240.1985 · DOI
  16. Lathia, 1975, Serotonin uptake and release by biochemically characterized nerve endings isolated from rat brain by concomitant flotation and sedimentation centrifugation, J Neural Transm, 37, 111, 10.1007/BF01663628 · DOI
  17. Duff, 2000, Characterization of pathology in transgenic mice over-expressing human genomic and cDNA tau transgenes, Neurobiol Dis, 7, 87, 10.1006/nbdi.1999.0279 · DOI · Paper page
  18. Greenberg, 1992, Hydrofluoric acid-treated tau PHF proteins display the same biochemical properties as normal tau, J Biol Chem, 267, 564, 10.1016/S0021-9258(18)48531-6 · DOI
  19. Watanabe, 1999, Deamidation and isoaspartate formation in smeared tau in paired helical filaments, J Biol Chem, 274, 7368, 10.1074/jbc.274.11.7368 · DOI
  20. Roberson, 2007, Reducing endogenous tau ameliorates amyloid beta-induced deficits in an Alzheimer's disease mouse model, Science, 316, 750, 10.1126/science.1141736 · DOI · Paper page
  21. Morales, 1989, Distribution of MAP2 in dendritic spines and its colocalization with actin: an immunogold electron-microscope study, Cell Tissue Res, 256, 447, 10.1007/BF00225592 · DOI
  22. Caceres, 1984, Differential subcellular localization of tubulin and the microtubule-associated protein MAP2 in brain tissue as revealed by immunocytochemistry with monoclonal hybridoma antibodies, J Neurosci, 4, 394, 10.1523/JNEUROSCI.04-02-00394.1984 · DOI
  23. Gordon-Weeks, 1982, Presynaptic microtubules: organisation and assembly/disassembly, Neuroscience, 7, 739, 10.1016/0306-4522(82)90079-3 · DOI
  24. Tai, 2008, Ubiquitin, the proteasome and protein degradation in neuronal function and dysfunction, Nat Rev Neurosci, 9, 826, 10.1038/nrn2499 · DOI · Paper page
  25. van Langenhove, 2012, The molecular basis of the frontotemporal lobar degeneration-amyotrophic lateral sclerosis spectrum, Ann Med, 10.3109/07853890.2012.665471 · DOI
  26. Benilova, 2012, The toxic Abeta oligomer and Alzheimer's disease: an emperor in need of clothes, Nat Neurosci, 15, 349, 10.1038/nn.3028 · DOI · Paper page
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  30. Dickey, 2006, Deletion of the ubiquitin ligase CHIP leads to the accumulation, but not the aggregation, of both endogenous phospho- and caspase-3-cleaved tau species, J Neurosci, 26, 6985, 10.1523/JNEUROSCI.0746-06.2006 · DOI · Paper page
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  32. Zhang, 2005, Microtubule-associated protein tau is a substrate of ATP/Mg(2+)-dependent proteasome protease system, J Neural Transm, 112, 547, 10.1007/s00702-004-0196-x · DOI
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Metadata

Authors
Tai, H.-C., Serrano-Pozo, A., Hashimoto, T., Frosch, M. P., Spires-Jones, T. L., & Hyman, B. T.
Venue
The American Journal of Pathology
Publisher
Elsevier BV
Published
2012-10
Volume
181
Issue
4
Pages
1426-1435
ISSN
0002-9440
DOI
10.1016/j.ajpath.2012.06.033
Cited by
443
References
11
Language
en
Licence
Funders
  • Fundación Alfonso Martín Escudero (AG08487, AG033670, P50 AG005134)
  • National Institutes of Health
  • American Health Assistance Foundation

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