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 language | English (US) |
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Pages (from-to) | 33-36 |
Number of pages | 4 |
Journal | Neuroscience Letters |
Volume | 252 |
Issue number | 1 |
DOIs | |
State | Published - Jul 27 1998 |
Externally published | Yes |
Keywords
- Alzheimer's disease
- Clathrin assembly protein AP180
- N- acetylglucosamine (O-GlcNAc)
- O-glycosylation
- Synaptic vesicle recycling
- Synaptophysin
ASJC Scopus subject areas
- General Neuroscience