The DOI matches its Crossref record; 7 of the 7 references it cites were found in a registry or an index.
Glucocerebrosidase is present in α-synuclein inclusions in Lewy body disorders
Open accessAbstract
Mutations in the gene encoding the lysosomal enzyme glucocerebrosidase, known to cause Gaucher disease (GD), are a risk factor for the development of Parkinson disease (PD) and related disorders. This association is based on the concurrence of parkinsonism and GD, the identification of glucocerebrosidase mutations in cohorts with PD from centers around the world, and neuropathologic findings. The contribution of glucocerebrosidase to the development of parkinsonian pathology was explored by studying seven brain samples from subjects carrying glucocerebrosidase mutations with pathologic diagnoses of PD and/or Lewy body dementia. Three individuals had GD and four were heterozygous for glucocerebrosidase mutations. All cases had no known family history of PD and the mean age of disease onset was 59 years (range 42–77). Immunofluorescence studies on brain tissue samples from patients with parkinsonism associated with glucocerebrosidase mutations showed that glucocerebrosidase was present in 32–90% of Lewy bodies (mean 75%), some ubiquitinated and others non-ubiquitinated. In samples from seven subjects without mutations, <10% of Lewy bodies were glucocerebrosidase positive (mean 4%). This data demonstrates that glucocerebrosidase can be an important component of α-synuclein-positive pathological inclusions. Unraveling the role of mutant glucocerebrosidase in the development of this pathology will further our understanding of the lysosomal pathways that likely contribute to the formation and/or clearance of these protein aggregates.
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Cites
Staging of brain pathology related to sporadic Parkinson’s disease
Braak, H., Tredici, K. D., Rüb, U., de Vos, R. A. I., Jansen Steur, E. N. H., & Braak, E. (2003) · Neurobiology of Aging · doi:10.1016/s0197-4580(02)00065-9 · Cited by 10,777
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Diagnosis and management of dementia with Lewy bodies: Third report of the DLB consortium
McKeith, I. G., Dickson, D. W., Lowe, J., Emre, M., O'Brien, J. T., Feldman, H., Cummings, J., Duda, J. E., Lippa, C., Perry, E. K., et al. (2005) · Neurology · doi:10.1212/01.wnl.0000187889.17253.b1 · Cited by 5,069
Multicenter Analysis of Glucocerebrosidase Mutations in Parkinson's Disease
Sidransky, E., Nalls, M. A., Aasly, J. O., Aharon-Peretz, J., Annesi, G., Barbosa, E. R., Bar-Shira, A., Berg, D., Bras, J., Brice, A., et al. (2009) · New England Journal of Medicine · doi:10.1056/nejmoa0901281 · Cited by 2,135
Self-citationImpaired Degradation of Mutant α-Synuclein by Chaperone-Mediated Autophagy
Cuervo, A. M., Stefanis, L., Fredenburg, R., Lansbury, P. T., & Sulzer, D. (2004) · Science · doi:10.1126/science.1101738 · Cited by 2,024 · cited 1×
“Furthermore, α-synuclein can be selectively translocated into the lysosomes for degradation by chaperone-mediated autophagy and aggregated forms of α-synuclein may be degraded by lysosomes [6].”
BackgroundMutations in the Glucocerebrosidase Gene and Parkinson's Disease in Ashkenazi Jews
Aharon-Peretz, J., Rosenbaum, H., & Gershoni-Baruch, R. (2004) · New England Journal of Medicine · doi:10.1056/nejmoa033277 · Cited by 597
Gai, W. P., Yuan, H. X., Li, X. Q., Power, J. T. H., Blumbergs, P. C., & Jensen, P. H. (2000) · Experimental Neurology · doi:10.1006/exnr.2000.7527 · Cited by 272
Cited by
Goedert, M., Spillantini, M. G., Del Tredici, K., & Braak, H. (2013) · Nature Reviews Neurology · doi:10.1038/nrneurol.2012.242 · Cited by 1,190
Schöndorf, D. C., Aureli, M., McAllister, F. E., Hindley, C. J., Mayer, F., Schmid, B., Sardi, S. P., Valsecchi, M., Hoffmann, S., Schwarz, L. K., et al. (2014) · Nature Communications · doi:10.1038/ncomms5028 · Cited by 543
Reduced glucocerebrosidase is associated with increased α-synuclein in sporadic Parkinson’s disease
Murphy, K. E., Gysbers, A. M., Abbott, S. K., Tayebi, N., Kim, W. S., Sidransky, E., Cooper, A., Garner, B., & Halliday, G. M. (2014) · Brain · doi:10.1093/brain/awt367 · Cited by 475
Self-citationDehay, B., Ramirez, A., Martinez-Vicente, M., Perier, C., Canron, M.-H., Doudnikoff, E., Vital, A., Vila, M., Klein, C., & Bezard, E. (2012) · Proceedings of the National Academy of Sciences · doi:10.1073/pnas.1112368109 · Cited by 379
Lysosomal impairment in Parkinson's disease
Dehay, B., Martinez‐Vicente, M., Caldwell, G. A., Caldwell, K. A., Yue, Z., Cookson, M. R., Klein, C., Vila, M., & Bezard, E. (2013) · Movement Disorders · doi:10.1002/mds.25462 · Cited by 340
Metadata
- Authors
- Goker-Alpan, O., Stubblefield, B. K., Giasson, B. I., & Sidransky, E.
- Venue
- Acta Neuropathologica
- Published
- 2010-09-14
- Volume
- 120
- Issue
- 5
- Pages
- 641-649
- ISSN
- 0001-6322 (ISSN-L)
- 1432-0533
- OpenAlex
- W1964353444
- Cited by
- 181
- References
- 7
- FWCI
- 10.84
- Type
- journal article
- Language
- en
- Open access
- green
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- Goker-Alpan, O., Stubblefield, B. K., Giasson, B. I., & Sidransky, E. (2010). Glucocerebrosidase is present in α-synuclein inclusions in Lewy body disorders. Acta Neuropathologica. https://doi.org/10.1007/s00401-010-0741-7
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