Cited by 533Alzheimer's disease research and treatmentsParkinson's Disease Mechanisms and TreatmentsDementia and Cognitive Impairment Research

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Lewy Bodies Contain Altered α-Synuclein in Brains of Many Familial Alzheimer's Disease Patients with Mutations in Presenilin and Amyloid Precursor Protein Genes

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Lippa, Carol F., Fujiwara, Hideo, Mann, David M.A., Giasson, Benoit, Baba, Minami, Schmidt, Marie L., Nee, Linda E., O'Connell, Brendan, Pollen, Dan A., St. George-Hyslop, Peter, Ghetti, Bernardino, Nochlin, David, Bird, Thomas D., Cairns, Nigel J., Lee, Virginia M.-Y., Iwatsubo, Takeshi, Trojanowski, John Q.·1998·The American Journal of Pathology

DOI 10.1016/s0002-9440(10)65722-7PMC PMC1853391

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Abstract

Missense mutations in the alpha-synuclein gene cause familial Parkinson's disease (PD), and alpha-synuclein is a major component of Lewy bodies (LBs) in sporadic PD, dementia with LBs (DLB), and the LB variant of Alzheimer's disease (AD). To determine whether alpha-synuclein is a component of LBs in familial AD (FAD) patients with known mutations in presenilin (n = 65) or amyloid precursor protein (n = 9) genes, studies were conducted with antibodies to alpha-, beta-, and gamma-synuclein. LBs were detected with alpha- but not beta- or gamma-synuclein antibodies in 22% of FAD brains, and alpha-synuclein-positive LBs were most numerous in amygdala where some LBs co-localized with tau-positive neurofibrillary tangles. As 12 (63%) of 19 FAD amygdala samples contained alpha-synuclein-positive LBs, these inclusions may be more common in FAD brains than previously reported. Furthermore, alpha-synuclein antibodies decorated LB filaments by immunoelectron microscopy, and Western blots revealed that the solubility of alpha-synuclein was reduced compared with control brains. The presence of alpha-synuclein-positive LBs was not associated with any specific FAD mutation. These studies suggest that insoluble alpha-synuclein aggregates into filaments that form LBs in many FAD patients, and we speculate that these inclusions may compromise the function and/or viability of affected neurons in the FAD brain.

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Authors: Lippa, C. F., Fujiwara, H., Mann, D. M. A., Giasson, B., Baba, M., Schmidt, M. L., Nee, L. E., O'Connell, B., Pollen, D. A., St. George-Hyslop, P., Ghetti, B., Nochlin, D., Bird, T. D., Cairns, N. J., Lee, V. M.-Y., Iwatsubo, T., & Trojanowski, J. Q.
Affiliations: The University of Tokyo (JP)
University of Manchester (GB)
University of Pennsylvania (US)
National Institute of Neurological Disorders and Stroke (US)
University of Massachusetts Chan Medical School (US)
Indiana University Hospital (US)
University of Washington (US)
Corresponding author: Lippa, Carol F.
ORCID: Lippa, Carol F.
Mann, David M.A.
Giasson, Benoit
Ghetti, Bernardino
Bird, Thomas D.
Cairns, Nigel J.
Lee, Virginia M.-Y.
Iwatsubo, Takeshi
Trojanowski, John Q.
Venue: The American Journal of Pathology
Publisher: Elsevier BV
Published: 1998-11
Volume: 153
Issue: 5
Pages: 1365-1370
ISSN: 0002-9440 (ISSN-L)
DOI: 10.1016/s0002-9440(10)65722-7
PMC: PMC1853391
OpenAlex: W2066155243
Cited by: 533
References: 35
Citations by year: 2026: 10 · 2025: 17 · 2024: 23 · 2023: 16 · 2022: 19 · 2021: 21 · 2020: 19 · 2019: 17 · 2018: 16 · 2017: 9 · 2016: 11 · 2015: 13 · 2014: 25 · 2013: 13 · 2012: 11
FWCI: 17.79
Type: journal article
Language: en
Open access: hybrid
doi.org
Licence: cc-by-nc-nd
www.elsevier.com/tdm/userlicense/1.0/ (tdm)
www.elsevier.com/legal/tdmrep-license (tdm)
creativecommons.org/licenses/by-nc-nd/4.0/ (vor, 4440 d)
Locations: American Journal Of Pathology (publishedVersion, cc-by-nc-nd)
PubMed Central (publishedVersion)
PubMed (publishedVersion)
Funders: National Institutes of Health (7r29ag013623-06)
National Institute on Aging (P30AG010133, AG09215, U01AG006781, AG13623, P30AG010124, P01AG009215, AG-10124, P50AG005136)
Topics: Life Sciences › Neuroscience › Cellular and Molecular Neuroscience › Alzheimer's disease research and treatments
Health Sciences › Medicine › Clinical Neurology › Parkinson's Disease Mechanisms and Treatments
Health Sciences › Medicine › Psychiatry and Mental health › Dementia and Cognitive Impairment Research
Keywords: Lewy bodies, alpha-synuclein, familial Alzheimer's disease, presenilin mutations, amyloid precursor protein mutations, amygdala, alpha-synuclein aggregation, protein insolubility, immunoelectron microscopy
MeSH terms: Adult, Aged, Alzheimer Disease, Brain, Female, Humans, Immunohistochemistry, Male, Membrane Proteins, Middle Aged, Mutation, Nerve Tissue Proteins, Blotting, Western, Microscopy, Immunoelectron, Amyloid beta-Protein Precursor, Lewy Bodies, Synucleins, alpha-Synuclein, gamma-Synuclein, Presenilin-1

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Lewy Bodies Contain Altered α-Synuclein in Brains of Many Familial Alzheimer's Disease Patients with Mutations in Presenilin and Amyloid Precursor Protein Genes

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