Affordable Access

Publisher Website

Relationship of phosphorylated α-synuclein and tau accumulation to Aβ deposition in the cerebral cortex of dementia with Lewy bodies

Experimental Neurology
Publication Date
DOI: 10.1016/j.expneurol.2007.11.019
  • Alzheimer'S Disease
  • Parkinson'S Disease
  • Neocortex
  • Amyloid
  • Neurite
  • Thread
  • Biology
  • Medicine


Abstract α-Synuclein accumulated in the brain of dementia with Lewy bodies (DLB) is phosphorylated at serine129 (pα-synuclein). We investigated the accumulation of pα-synuclein in the brains of patients with DLB and Alzheimer's disease (AD). We employed 18 DLB patients with neocortical Lewy body type pathology (nLBTP) with or without AD. We also employed the same number of AD cases without significant nLBTP. We refer to the former group as the nLBTP group and to the latter as the AD type pathology (ADTP) group. In the nLBTP group, pα-synuclein positive neurite pathology such as threads and dots occurs in all layers of the temporal neocortex. It was comparable in degree with tau pathology in AD. Fifteen cases in the nLBTP group were associated with Aβ deposition that meets the CERAD plaque score “C” and one case with a score “B”. In these plaque-associated cases, the severity of pα-synuclein pathology was related to the degree of Aβ deposition. In the cases with relatively moderate Aβ deposition, tau pathology was disproportionately mild in the nLBTP group, while the total of tau and pα-synuclein pathology was proportionate to Aβ deposition in both the nLBTP and ADTP groups. Our results support the ideas that there is an overlap in the pathology between AD and DLB and that Aβ promotes accumulation of both α-synuclein and tau. The procession from Aβ to neurite pathology in the cerebral cortex of AD and DLB may be unifiable.

There are no comments yet on this publication. Be the first to share your thoughts.