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Increase of -Synuclein Aggregates in Neurodegenerative Diseases With Tau-Based Inclusions

Anca Popescu, MD; Carol F. Lippa, MD; Virginia M.-Y. Lee, PhD; John Q. Trojanowski, MD, PhD

Arch Neurol. 2004;61:1915-1919.

Background  Increased attention has been given to -synuclein aggregation in nonsynucleinopathies because -synuclein–containing Lewy bodies (LBs) influence symptoms. However, the spectrum of disorders in which secondary inclusions are likely to occur has not been defined. Amygdala neurons commonly develop large numbers of secondary LBs, making it a practical region for studying this phenomenon.

Objective  To characterize the spectrum of diseases associated with LB formation in the amygdala of neurodegenerative disease and control cases.

Design  An autopsy series of 101 neurodegenerative disease and 34 aged control cases. Using immunohistochemistry studies, we examined the amygdala for -synuclein aggregates.

Results  Lewy bodies were often abundant in classic Pick disease, argyrophilic grain disease, Alzheimer disease, and dementia with LBs but not in cases with amygdala degeneration lacking tau-based inclusions, control cases, preclinical disease carriers, or degenerative diseases lacking pathologic involvement of the amygdala. The exposed -synuclein epitopes were similar in all cases containing LBs.

Conclusions  Abnormal -synuclein aggregation in the amygdala is disease selective, but not restricted to disorders of -synuclein and -amyloid. Our data are compatible with the notion that tau aggregates predispose neurons to develop secondary LBs.

Author Affiliations: Department of Neurology, Drexel University College of Medicine (Drs Popescu and Lippa), and Center for Neurodegenerative Disease Research, University of Pennsylvania School of Medicine (Drs Lee and Trojanowski), Philadelphia.

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