The DOI matches its Crossref record; 31 of the 31 references it cites were found in a registry or an index.
Activation and redistribution of c‐Jun N‐terminal kinase/stress activated protein kinase in degenerating neurons in Alzheimer's disease
Abstract
Cellular responses to increased oxidative stress appear to be a mechanism that contributes to the varied cytopathology of Alzheimer's disease (AD). In this regard, we suspect that c‐Jun N‐terminal kinase/Stress activated protein kinase (JNK/SAPK), a major cellular stress response protein induced by oxidative stress, plays an important role in Alzheimer disease in susceptible neurons facing the dilemma of proliferation or death. We found that JNK2/SAPK‐α and JNK3/SAPK‐β were related to neurofibrillary pathology and JNK1/SAP‐Kγ related to Hirano bodies in cases of AD but were only weakly diffuse in the cytoplasm in all neurons in control cases and in non‐involved neurons in diseased brain. In this regard, in hippocampal and cortical regions of individuals with severe AD, the activated phospho‐JNK/SAPK was localized exclusively in association with neurofibrillar alterations including neurofibrillary tangles, senile plaque neurites, neuropil threads and granulovacuolar degeneration structures (GVD), completely overlapping with τ‐positive neurofibrillary pathology, but was virtually absent in these brain regions in younger and age‐matched controls without pathology. However, in control patients with some pathology, as well as in mild AD cases, there was nuclear phospho‐JNK/SAPK and translocation of phospho‐JNK/SAPK from nuclei to cytoplasm, respectively, indicating that the activation and re‐distribution of JNK/SAPK correlates with the progress of the disease. By immunoblot analysis, phospho‐JNK/SAPK is significantly increased in AD over control cases. Together, these findings suggest that JNK/SAPK dysregulation, probably resulting from oxidative stress, plays an important role in the increased phosphorylation of cytoskeletal proteins found in AD.
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Cites
Mirra, S. S., Heyman, A., McKeel, D., Sumi, S. M., Crain, B. J., Brownlee, L. M., Vogel, F. S., Hughes, J. P., Belle, G. V., Berg, L., et al. (1991) · Neurology · doi:10.1212/wnl.41.4.479 · Cited by 4,961
Diagnosis of Alzheimer's Disease
Khachaturian, Z. S. (1985) · Archives of Neurology · doi:10.1001/archneur.1985.04060100083029 · Cited by 2,499 · cited 1×
“All cases were categorized based on clinical and pathological criteria established by CERAD and an NIA consensus panel (Khachaturian 1985; Mirra et al. 1991).”
MethodMitogen-activated protein kinase pathways
Robinson, M. J., & Cobb, M. H. (1997) · Current Opinion in Cell Biology · doi:10.1016/s0955-0674(97)80061-0 · Cited by 2,474
Sayre, L. M., Zelasko, D. A., Harris, P. L. R., Perry, G., Salomon, R. G., & Smith, M. A. (1997) · Journal of Neurochemistry · doi:10.1046/j.1471-4159.1997.68052092.x · Cited by 1,007
Self-citationOxidative damage in Alzheimer's
Smith, M. A., Perry, G., Richey, P. L., Sayrec, L. M., Anderson, V. E., Beal, M. F., & Kowall, N. (1996) · Nature · doi:10.1038/382120b0 · Cited by 894
Self-citationCobb, M. H. (1999) · Progress in Biophysics and Molecular Biology · doi:10.1016/s0079-6107(98)00056-x · Cited by 875
Mitogen-activated protein kinase cascades and regulation of gene expression
Su, B., & Karin, M. (1996) · Current Opinion in Immunology · doi:10.1016/s0952-7915(96)80131-2 · Cited by 747
RNA Oxidation Is a Prominent Feature of Vulnerable Neurons in Alzheimer’s Disease
Nunomura, A., Perry, G., Pappolla, M. A., Wade, R., Hirai, K., Chiba, S., & Smith, M. A. (1999) · The Journal of Neuroscience · doi:10.1523/jneurosci.19-06-01959.1999 · Cited by 722
Self-citationAdvanced Maillard reaction end products are associated with Alzheimer disease pathology.
Smith, M. A., Taneda, S., Richey, P. L., Miyata, S., Yan, S. D., Stern, D., Sayre, L. M., Monnier, V. M., & Perry, G. (1994) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.91.12.5710 · Cited by 714
Self-citationRegulation and function of the JNK subgroup of MAP kinases
Minden, A., & Karin, M. (1997) · Biochimica et Biophysica Acta (BBA) - Reviews on Cancer · doi:10.1016/s0304-419x(97)00018-8 · Cited by 484
Cited by
Neuropathological alterations in Alzheimer disease
Serrano-Pozo, A., Frosch, M. P., Masliah, E., & Hyman, B. T. (2011) · Cold Spring Harbor Perspectives in Medicine · doi:10.1101/cshperspect.a006189 · Cited by 3,345
Mitochondrial abnormalities in Alzheimer's disease
Hirai, K., Aliev, G., Nunomura, A., Fujioka, H., Russell, R. L., Atwood, C. S., Johnson, A. B., Kress, Y., Vinters, H. V., Tabaton, M., et al. (2001) · The Journal of Neuroscience · doi:10.1523/jneurosci.21-09-03017.2001 · Cited by 1,367
Self-citationMolecular inflammation: Underpinnings of aging and age-related diseases
Chung, H. Y., Cesari, M., Anton, S., Marzetti, E., Giovannini, S., Seo, A. Y., Carter, C., Yu, B. P., & Leeuwenburgh, C. (2009) · Ageing Research Reviews · doi:10.1016/j.arr.2008.07.002 · Cited by 1,203
Oxidative Stress and the Pathogenesis of Alzheimer's Disease
Zhao, Y., & Zhao, B. (2013) · Oxidative Medicine and Cellular Longevity · doi:10.1155/2013/316523 · Cited by 855
Molecular mechanisms of neurodegeneration in Alzheimer's disease
Crews, L., & Masliah, E. (2010) · Human Molecular Genetics · doi:10.1093/hmg/ddq160 · Cited by 772
Metadata
- Authors
- Zhu, X., Raina, A. K., Rottkamp, C. A., Aliev, G., Perry, G., Boux, H., & Smith, M. A.
- Venue
- Journal of Neurochemistry
- Publisher
- Wiley
- Published
- 2001-01
- Volume
- 76
- Issue
- 2
- Pages
- 435-441
- ISSN
- 0022-3042 (ISSN-L)
- 1471-4159
- OpenAlex
- W2042347168
- Cited by
- 421
- References
- 31
- FWCI
- 17.31
- Type
- journal article
- Language
- en
- Open access
- closed
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