[email protected]; Ki Wan Oh – [email protected]; Jin Tae Hong* – [email protected] * Corresponding authorPublished: 29 August 2008 Journal of Neuroinflammation 2008, 5:37 doi:10.1186/1742-2094-5-Received: 22 March 2008 Accepted: 29 AugustThis article is available from: http://www.jneuroinflammation/content/5/1/37 2008 Lee et al; licensee BioMed Central Ltd. This is an Open Access article distributed under the terms of the Creative Commons Attribution License (http://creativecommons.org/licenses/by/2.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.AbstractBackground: Alzheimer’s disease (AD) is characterized by extensive loss of neurons in the brain of AD patients. Intracellular accumulation of beta-amyloid peptide (A) has also shown to occur in AD. Neuro-inflammation has been known to play a role in the pathogenesis of AD. Methods: In this study, we investigated neuro-inflammation and amyloidogenesis and memory impairment following the systemic inflammation generated by lipopolysaccharide (LPS) using immunohistochemistry, ELISA, behavioral tests and Western blotting.IL-1 beta Protein, Human Results: Intraperitoneal injection of LPS, (250 g/kg) induced memory impairment determined by passive avoidance and water maze tests in mice.Pyrroloquinoline quinone Repeated injection of LPS (250 g/kg, 3 or 7 times) resulted in an accumulation of A12 in the hippocampus and cerebralcortex of mice brains through increased – and -secretase activities accompanied with the increased expression of amyloid precursor protein (APP), 99-residue carboxy-terminal fragment of APP (C99) and generation of A12 as well as activation of astrocytes in vivo. 3 weeks of pretreatment of sulindac sulfide (3.PMID:23776646 75 and 7.5 mg/kg, orally), an anti-inflammatory agent, suppressed the LPS-induced amyloidogenesis, memory dysfunction as well as neuronal cell death in vivo. Sulindac sulfide (12.550 M) also suppressed LPS (1 g/ml)-induced amyloidogenesis in cultured neurons and astrocytes in vitro. Conclusion: This study suggests that neuro-inflammatory reaction could contribute to AD pathology, and anti-inflammatory agent could be useful for the prevention of AD.BackgroundAlzheimer’s disease (AD) is a progressive neuro-psychiatric disorder. The major neuropathological hallmarks of AD are the formation of senile plaques (SPs) followingneurofibrillary tangles (NFTs) which cause neuronal degeneration and synaptic loss. SPs are extracellular deposits of fibrillar and amorphous aggregates of amyloid beta-peptide (A) whereas NFTs are intracellular fibrillarPage 1 of(page number not for citation purposes)Journal of Neuroinflammation 2008, 5:http://www.jneuroinflammation/content/5/1/aggregates of the microtubule-associated protein tau that exhibit hyperphosphorylation. The formation of SPs and NFTs in brain regions such as the entorhinal cortex, hippocampus, basal forebrain and amygdala impaired learning and memory functions [1]. AD brains also exhibit a number of pathological abnormalities, including a profound loss of synapses, reactive gliosis, and inflammatory processes [2]. The brain has an endogenous immune system that is coordinated by immunocompetent cells such as microglia. The brain is also vulnerable to constitutive defense responses, such as inflammation [3,4]. The inflammation associated with the brain, neuro-inflammation, differs from that found in the periphery. Although edema and neutrophil invasion, typical features of inflammation, i.