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Neurotoxicity and synaptic plasticity impairment of N-acetylglucosamine polymers: implications for Alzheimer's disease.

Abstract：

:We assessed whether polymers of N-acetylglucosamine (GlcNAc) have any pathogenetic role in Alzheimer's disease (AD). First, by using specific dyes, we found deposits of polymers of GlcNAc in sporadic but not in familial AD. We found that neurons and microglia exposed to GlcNAc and uridine diphosphate (UDP)-GlcNAc are able to form GlcNAc polymers, which display a significant neurotoxicity in vitro. Moreover, the exposure of organotypic hippocampal cultures to the same compounds led to synaptic impairment with decreased levels of syntaxin and synaptophysin. In addition, acute hippocampal slices treated with GlcNAc/UDP-GlcNAc showed a clear reduction of long-term potentiation of excitatory synapses. Finally, we demonstrated that microglial cells are able to phagocytose chitin particles and, when exposed to GlcNAc/UDP-GlcNAc, show cellular activation and intracellular deposition of GlcNAc polymers that are eventually released in the extracellular space. Taken together, our results indicate that both microglia and neurons produce GlcNAc polymers, which trigger neurotoxicity both directly and through microglia activation. GlcNAc polymer-driven neurotoxicity offers novel pathogenic insights in sporadic AD and new therapeutic options.

journal_name

Neurobiol Aging

journal_title

Neurobiology of aging

authors

Turano E,Busetto G,Marconi S,Guzzo F,Farinazzo A,Commisso M,Bistaffa E,Angiari S,Musumeci S,Sotgiu S,Bonetti B

doi

10.1016/j.neurobiolaging.2014.12.033

subject

Has Abstract

pub_date

2015-05-01 00:00:00

pages

1780-91

issue

5

eissn

0197-4580

issn

1558-1497

pii

S0197-4580(14)00850-1

journal_volume

36

pub_type

杂志文章

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