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Incidental Lewy body disease and preclinical Parkinson disease.
Arch Neurol. 2008 Aug; 65(8):1074-80.AN

Abstract

BACKGROUND

The significance of Lewy bodies detected at autopsy in the brains of clinically normal individuals is uncertain but may represent preclinical Parkinson disease (PD).

OBJECTIVE

To determine whether diminished striatal dopaminergic innervation and nigral cell loss are present in incidental Lewy body disease (iLBD), as one might expect if it is a forerunner of PD.

DESIGN

Case-control study.

SETTING

Medical records and archival brain tissue were obtained from a tertiary medical center for further study.

PARTICIPANTS

Brains from clinically healthy individuals older than 60 years with alpha-synuclein-immunoreactive Lewy bodies (iLBD; n = 12) were compared with those from clinically healthy individuals with no alpha-synuclein pathologic findings (n = 31) and patients with PD (n = 25).

MAIN OUTCOME MEASURES

Striatal dopaminergic integrity assessed in sections of putamen by immunofluorescence for tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT2), neuronal loss score in the substantia nigra, and distribution of Lewy bodies according to PD stage.

RESULTS

Among the participants with iLBD, decreased striatal dopaminergic immunoreactivity was documented for both TH (33%) and VMAT2 (42%), compared with the pathologically normal subjects; as expected, the reductions were even greater in PD (73% decrease for TH and 96% decrease for VMAT2). Substantia nigra neuronal loss inversely correlated with both striatal TH (r = -0.84) and VMAT2 (r = -0.77). In addition, PD stage inversely correlated with both striatal VMAT2 (r = -0.85) and TH (r = -0.85).

CONCLUSIONS

The results indicate that iLBD has nigrostriatal pathological features that are intermediate between those in pathologically normal persons and those with PD. The findings suggest that iLBD probably represents presymptomatic PD, rather than nonspecific, age-related alpha-synuclein pathological changes.

Authors+Show Affiliations

Department of Neuroscience, Mayo Clinic, Jacksonville, FL 32224, USA.No affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info availableNo affiliation info available

Pub Type(s)

Comparative Study
Journal Article
Research Support, N.I.H., Extramural
Research Support, Non-U.S. Gov't

Language

eng

PubMed ID

18695057

Citation

DelleDonne, Anthony, et al. "Incidental Lewy Body Disease and Preclinical Parkinson Disease." Archives of Neurology, vol. 65, no. 8, 2008, pp. 1074-80.
DelleDonne A, Klos KJ, Fujishiro H, et al. Incidental Lewy body disease and preclinical Parkinson disease. Arch Neurol. 2008;65(8):1074-80.
DelleDonne, A., Klos, K. J., Fujishiro, H., Ahmed, Z., Parisi, J. E., Josephs, K. A., Frigerio, R., Burnett, M., Wszolek, Z. K., Uitti, R. J., Ahlskog, J. E., & Dickson, D. W. (2008). Incidental Lewy body disease and preclinical Parkinson disease. Archives of Neurology, 65(8), 1074-80. https://doi.org/10.1001/archneur.65.8.1074
DelleDonne A, et al. Incidental Lewy Body Disease and Preclinical Parkinson Disease. Arch Neurol. 2008;65(8):1074-80. PubMed PMID: 18695057.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Incidental Lewy body disease and preclinical Parkinson disease. AU - DelleDonne,Anthony, AU - Klos,Kevin J, AU - Fujishiro,Hiroshige, AU - Ahmed,Zeshan, AU - Parisi,Joseph E, AU - Josephs,Keith A, AU - Frigerio,Roberta, AU - Burnett,Melinda, AU - Wszolek,Zbigniew K, AU - Uitti,Ryan J, AU - Ahlskog,J Eric, AU - Dickson,Dennis W, PY - 2008/8/13/pubmed PY - 2008/9/17/medline PY - 2008/8/13/entrez SP - 1074 EP - 80 JF - Archives of neurology JO - Arch Neurol VL - 65 IS - 8 N2 - BACKGROUND: The significance of Lewy bodies detected at autopsy in the brains of clinically normal individuals is uncertain but may represent preclinical Parkinson disease (PD). OBJECTIVE: To determine whether diminished striatal dopaminergic innervation and nigral cell loss are present in incidental Lewy body disease (iLBD), as one might expect if it is a forerunner of PD. DESIGN: Case-control study. SETTING: Medical records and archival brain tissue were obtained from a tertiary medical center for further study. PARTICIPANTS: Brains from clinically healthy individuals older than 60 years with alpha-synuclein-immunoreactive Lewy bodies (iLBD; n = 12) were compared with those from clinically healthy individuals with no alpha-synuclein pathologic findings (n = 31) and patients with PD (n = 25). MAIN OUTCOME MEASURES: Striatal dopaminergic integrity assessed in sections of putamen by immunofluorescence for tyrosine hydroxylase (TH) and vesicular monoamine transporter 2 (VMAT2), neuronal loss score in the substantia nigra, and distribution of Lewy bodies according to PD stage. RESULTS: Among the participants with iLBD, decreased striatal dopaminergic immunoreactivity was documented for both TH (33%) and VMAT2 (42%), compared with the pathologically normal subjects; as expected, the reductions were even greater in PD (73% decrease for TH and 96% decrease for VMAT2). Substantia nigra neuronal loss inversely correlated with both striatal TH (r = -0.84) and VMAT2 (r = -0.77). In addition, PD stage inversely correlated with both striatal VMAT2 (r = -0.85) and TH (r = -0.85). CONCLUSIONS: The results indicate that iLBD has nigrostriatal pathological features that are intermediate between those in pathologically normal persons and those with PD. The findings suggest that iLBD probably represents presymptomatic PD, rather than nonspecific, age-related alpha-synuclein pathological changes. SN - 1538-3687 UR - https://www.unboundmedicine.com/medline/citation/18695057/Incidental_Lewy_body_disease_and_preclinical_Parkinson_disease_ L2 - https://jamanetwork.com/journals/jamaneurology/fullarticle/10.1001/archneur.65.8.1074 DB - PRIME DP - Unbound Medicine ER -