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Neurochem Res. 2012 May;37(5):903-10. doi: 10.1007/s11064-012-0708-2. Epub 2012 Feb 7.

Neuroinflammation and synaptic loss.

Author information

1
Brain Physiology and Metabolism Section, National Institute on Aging, National Institutes of Health, Bldg. 9, Rm. 1S126 MSC 0947, Bethesda, MD 20892-0947, USA. jrao@grc.nia.nih.gov

Abstract

Neuroinflammation plays a critical role in the progression of many neurodegenerative, neuropsychiatric and viral diseases. In neuroinflammation, activated microglia and astrocytes release cytokines and chemokines as well as nitric oxide, which in turn activate many signal transduction pathways. The cytokines, interleukin-1 beta and tumor necrosis factor alpha, regulate transcription of a number of genes within the brain, which can lead to the formation of pro-inflammatory products of the arachidonic acid cascade. Formation of pro-inflammatory agents and associated cytotoxic products during neuroinflammation can be detrimental to neurons by altering synaptic proteins. Neuroinflammation as well as excitotoxic insults reduce synaptic markers such as synaptophysin and drebrin. Neurodegenerative, neuropsychiatric illnesses and viral infections are accompanied by loss of both pre- and post-synaptic proteins. These synaptic changes may contribute to the progressive cognitive decline and behavioral changes associated with these illnesses.

PMID:
22311128
PMCID:
PMC3478877
DOI:
10.1007/s11064-012-0708-2
[Indexed for MEDLINE]
Free PMC Article

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