Reduced O-glycosylated clathrin assembly protein AP180: Implication for synaptic vesicle recycling dysfunction in Alzheimer's disease

Pamela J. Yao, Paul D. Coleman

Research output: Contribution to journalArticle

50 Scopus citations

Abstract

Synapse loss is one of the neuropathotogies in Alzheimer's disease (AD) that may play a crucial role in the mechanism of its distinct cognitive impairment and dementia. In a previous study [18], a significant reduction of O-glycosylated clathrin assembly protein AP180 was observed in neocortex of AD. The reduction correlated with the density of neurofibrillary tangles. In this study we further determine that the O-GIcNAc/AP180 ratio is not changed, but the level of AP180 protein decreases in. Further more, whereas the level of neurofilament (NF-M) remains relatively unchanged, another clathrin assembly protein, AP-2, is also reduced in AD along with a small loss of synaptophysin. Our findings suggest that synaptic vesicle recycling dysfunction may be involved in the pathology of synapse loss in AD.

Original languageEnglish (US)
Pages (from-to)33-36
Number of pages4
JournalNeuroscience Letters
Volume252
Issue number1
DOIs
StatePublished - Jul 27 1998
Externally publishedYes

Keywords

  • Alzheimer's disease
  • Clathrin assembly protein AP180
  • N- acetylglucosamine (O-GlcNAc)
  • O-glycosylation
  • Synaptic vesicle recycling
  • Synaptophysin

ASJC Scopus subject areas

  • Neuroscience(all)

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