Accumulation of Insoluble α-Synuclein in Dementia with Lewy Bodies

Bruce C.V. Campbell; Qiao-Xin Li; Janetta G. Culvenor; Pekka Jäkälä; Roberto Cappai; Konrad Beyreuther; Colin L. Masters; Catriona A. McLean

Neurobiology of Disease (Jun 2000)

Accumulation of Insoluble α-Synuclein in Dementia with Lewy Bodies

Bruce C.V. Campbell,
Qiao-Xin Li,
Janetta G. Culvenor,
Pekka Jäkälä,
Roberto Cappai,
Konrad Beyreuther,
Colin L. Masters,
Catriona A. McLean

Affiliations

Bruce C.V. Campbell: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Qiao-Xin Li: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Janetta G. Culvenor: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Pekka Jäkälä: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Roberto Cappai: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Konrad Beyreuther: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Colin L. Masters: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland
Catriona A. McLean: Department of Pathology, The University of Melbourne, 3010, Australia; The Mental Health Research Institute of Victoria, Parkville, 3052, Australia; Centre for Molecular Biology, The University of Heidelberg, D69120, Germany; University and University Hospital of Kuopio, FIN-70211, Kuopio, Finland

Journal volume & issue: Vol. 7, no. 3
pp. 192 – 200

Abstract

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The α-synuclein (αSN) protein is thought to play a central role in the pathogenesis of neurodegenerative diseases where it aggregates to form intracellular inclusions. We have used Western blotting to examine the expression levels and solubility of αSN in brain homogenates from dementia with Lewy bodies (DLB), Parkinson's disease (PD), Alzheimer's disease (AD), and normal controls using samples from the parahippocampus/transentorhinal cortex. Compared to controls, DLB brains accumulate significantly greater amounts of sodium dodecyl sulfate (SDS)-soluble and SDS-insoluble αSN but levels of TBS-soluble αSN did not change. Levels of synaptophysin, a marker of synaptic integrity, were significantly lower in DLB cases than in normal aged controls regardless of whether concurrent changes of AD were present. This limbic synaptic dysfunction may contribute to cognitive impairment in DLB. Whether aggregated αSN is a cause or effect of the disease process in DLB and PD remains to be determined, but the presence of aggregated αSN is consistent with a pathogenesis similar to that associated with aggregates of Aβ amyloid in AD.

Published in Neurobiology of Disease

ISSN: 0969-9961 (Print); 1095-953X (Online)
Publisher: Elsevier
Country of publisher: United States
LCC subjects: Medicine: Internal medicine: Neurosciences. Biological psychiatry. Neuropsychiatry
Website: https://www.journals.elsevier.com/neurobiology-of-disease

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