Journal
NEUROSCIENCE LETTERS
Volume 322, Issue 2, Pages 75-78Publisher
ELSEVIER SCI IRELAND LTD
DOI: 10.1016/S0304-3940(02)00087-3
Keywords
neuroinflammation; beta-amyloid; thiorphan; Alzheimer's disease
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Funding
- NIA NIH HHS [AG10546] Funding Source: Medline
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Beta-amyloid deposition and neuroinflammation are two important features of Alzheimer's disease (AD) that may influence its progression. Chronic infusion of lipopolysaccharide (LPS) into the rodent 4th ventricle reproduces many of the neurobiological changes seen in AD. Chronic infusion of ascorbic acid containing thiorphan, an inhibitor of the enzyme neprilysin that catabolizes beta-amyloid, into the hippocampus induces extracellular deposition of beta-amyloid fibrils. We investigated whether the combined presence of chronic neuroinflammation could exacerbate the deposition of beta-amyloid induced by thiorphan. The infusion of any solution containing ascorbic acid alone or with thiorphan or LPS increased the level of intraneuronal beta-amyloid immunoreactivity. Solutions that did not contain ascorbic acid were not associated with increased intraneuronal beta-amyloid immunoreactivity. The role of neprilysin in the deposition of beta-amyloid in AD brains remains undetermined. (C) 2002 Elsevier Science Ireland Ltd. All rights reserved.
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