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Lewy body pathology in Alzheimer's disease.
J Mol Neurosci. 2001 Oct; 17(2):225-32.JM

Abstract

Lewy bodies, the characteristic pathological lesion of substantia nigra neurons in Parkinson's disease (PD), are frequently observed to accompany the amyloid plaque and neurofibrillary tangle pathology of Alzheimer's disease (AD). However the typical anatomic distribution of Lewy bodies in AD is distinct from PD. The most common site of occurrence is the amygdala, where Lewy bodies are observed in approximately 60% of both sporadic and familial AD. Other common sites of occurrence include the periamygdaloid and entorhinal cortex, while neocortical and brainstem areas develop Lewy bodies in a lower percentage of cases. In contrast, dementia with Lewy bodies (DLB), defined by widespread neocortical and brainstem Lewy bodies but frequently accompanied by variable levels of AD-type pathology, represents the other end of a spectrum of pathology associated with dementia. The observation of Lewy bodies in familial AD cases suggests that like neurofibrillary tangles, the formation of Lewy bodies can be induced by the pathological state caused by Abeta-amyloid overproduction. The role of Lewy body formation in the dysfunction and degeneration of neurons remains unclear. The protein alpha-synuclein appears to be an important structural component of Lewy bodies, an observation spurred by the discovery of point mutations in the alpha-synuclein gene linked to rare cases of autosomal dominant PD. Further investigation of alpha-synuclein and its relationship to pathological conditions promoting Lewy body formation in AD, PD, and DLB may yield further insight into pathogenesis of these diseases.

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Authors+Show Affiliations

Kotzbauer PT
Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine, Philadelphia, USA.
Trojanowsk JQ
No affiliation info available
Lee VM
No affiliation info available

MeSH

Alzheimer DiseaseAmyloid beta-PeptidesAnimalsBrainHumansLewy BodiesNerve Tissue ProteinsNeuronsOxidative StressPoint MutationSynucleinsalpha-Synucleintau Proteins

Pub Type(s)

Journal Article
Review

Language

eng

PubMed ID

11816795

Citation

Kotzbauer, P T., et al. "Lewy Body Pathology in Alzheimer's Disease." Journal of Molecular Neuroscience : MN, vol. 17, no. 2, 2001, pp. 225-32.
Kotzbauer PT, Trojanowsk JQ, Lee VM. Lewy body pathology in Alzheimer's disease. J Mol Neurosci. 2001;17(2):225-32.
Kotzbauer, P. T., Trojanowsk, J. Q., & Lee, V. M. (2001). Lewy body pathology in Alzheimer's disease. Journal of Molecular Neuroscience : MN, 17(2), 225-32.
Kotzbauer PT, Trojanowsk JQ, Lee VM. Lewy Body Pathology in Alzheimer's Disease. J Mol Neurosci. 2001;17(2):225-32. PubMed PMID: 11816795.
* Article titles in AMA citation format should be in sentence-case
TY - JOUR T1 - Lewy body pathology in Alzheimer's disease. AU - Kotzbauer,P T, AU - Trojanowsk,J Q, AU - Lee,V M, PY - 2002/1/31/pubmed PY - 2002/5/8/medline PY - 2002/1/31/entrez SP - 225 EP - 32 JF - Journal of molecular neuroscience : MN JO - J Mol Neurosci VL - 17 IS - 2 N2 - Lewy bodies, the characteristic pathological lesion of substantia nigra neurons in Parkinson's disease (PD), are frequently observed to accompany the amyloid plaque and neurofibrillary tangle pathology of Alzheimer's disease (AD). However the typical anatomic distribution of Lewy bodies in AD is distinct from PD. The most common site of occurrence is the amygdala, where Lewy bodies are observed in approximately 60% of both sporadic and familial AD. Other common sites of occurrence include the periamygdaloid and entorhinal cortex, while neocortical and brainstem areas develop Lewy bodies in a lower percentage of cases. In contrast, dementia with Lewy bodies (DLB), defined by widespread neocortical and brainstem Lewy bodies but frequently accompanied by variable levels of AD-type pathology, represents the other end of a spectrum of pathology associated with dementia. The observation of Lewy bodies in familial AD cases suggests that like neurofibrillary tangles, the formation of Lewy bodies can be induced by the pathological state caused by Abeta-amyloid overproduction. The role of Lewy body formation in the dysfunction and degeneration of neurons remains unclear. The protein alpha-synuclein appears to be an important structural component of Lewy bodies, an observation spurred by the discovery of point mutations in the alpha-synuclein gene linked to rare cases of autosomal dominant PD. Further investigation of alpha-synuclein and its relationship to pathological conditions promoting Lewy body formation in AD, PD, and DLB may yield further insight into pathogenesis of these diseases. SN - 0895-8696 UR - https://www.unboundmedicine.com/medline/citation/11816795/Lewy_body_pathology_in_Alzheimer's_disease_ L2 - https://dx.doi.org/10.1385/jmn:17:2:225 DB - PRIME DP - Unbound Medicine ER -