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Publication Detail
Neuronal and Peripheral pentraxins modify glutamate release and may interact in blood-brain barrier failure
  • Publication Type:
    Journal article
  • Publication Sub Type:
    Article
  • Authors:
    Cummings DM, Benway TA, Ho H, Tedoldi A, Fernandes Freitas MM, Shahab L, Murray CE, Richard-Londt A, Brandner S, Lashley TA, Salih DA, Edwards FA
  • Publisher:
    Oxford University Press (OUP): Policy B
  • Publication date:
    01/06/2017
  • Journal:
    Cerebral Cortex
  • Print ISSN:
    1460-2199
Abstract
Neuronal pentraxin 1 (NPTX1) has been implicated in Alzheimer’s disease, being present in and around dystrophic neurones in plaques, affecting glutamatergic transmission postsynaptically and mediating effects of amyloidβ. Here we confirm the presence of NPTX1 around plaques in post-mortem Alzheimer’s disease brain and report that acutely applied human NPTX1 increases paired-pulse ratio at mouse CA3-CA1 hippocampal synapses, indicating a decrease in glutamate release. In contrast, chronic exposure to NPTX1, NPTX2 or NPTX receptor decreases paired-pulse ratio, mimicking some of the earliest changes in mice expressing familial Alzheimer’s disease genes. The peripheral pentraxin, serum amyloid P component (SAP), causes similar synaptic effects to NPTX1. The presence of SAP on amyloid plaques in Alzheimer’s disease confirms that it can enter the brain. We show that SAP and neuronal pentraxins can interact and that SAP can enter the brain if the blood-brain barrier is compromised, suggesting that peripheral pentraxins could affect central synaptic transmission via this interaction, especially in the event of blood-brain barrier breakdown.
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