α-synuclein aggregation in pathological aging and Alzheimer's disease: The impact of β-amyloid plaque level

Abstract

In central nervous system diseases, abnormal aggregation of one protein is often associated with aggregation of other proteins. To begin to assess whether β-amyloid (Aβ) is associated with α-synuclein (AS) aggregation [secondary Lewy body (LB) formation], we used immunohistochemical techniques to compare the amygdala of 11 subjects with pathological aging and 18 with Alzheimer's disease. Overall, Aβ-40 plaque level was greater in cases with secondary AS aggregates. Aβ-42 plaque level was not associated with AS aggregation. Aβ-40 plaque levels cannot be ruled out as a factor involved in secondary LB formation.