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Beneficial effects of tri-lithium pyrroloquinoline quinonein on behaviors and pathology in a mouse model of Alzheimer’s disease

Authors
Journal
Molecular Neurodegeneration
1750-1326
Publisher
Springer (Biomed Central Ltd.)
Publication Date
Volume
7
Identifiers
DOI: 10.1186/1750-1326-7-s1-o14
Keywords
  • Oral Presentation
Disciplines
  • Biology
  • Medicine

Abstract

Beneficial effects of tri-lithium pyrroloquinoline quinonein on behaviors and pathology in a mouse model of Alzheimer’s disease ORAL PRESENTATION Open Access Beneficial effects of tri-lithium pyrroloquinoline quinonein on behaviors and pathology in a mouse model of Alzheimer’s disease Lei Zhao1, Neng Gong2, Xiaojing Sun1, Zhe Yu2, Qi Fang2, Na Zhao1, Xiaoli Pan1, Tianle Xu2*, Chunjiu Zhong1* From 2011 International Conference on Molecular Neurodegeneration Shanghai, China. 22-24 September 2011 Alzheimer’s disease (AD) is a complex disease with char- acteristic pathological hallmarks of senile plaques and neurofibrillary tangles, the occurrence and development of which are involved in multiple neurodegenerative pro- cesses. Conventional AD therapies target only at single disease-causing mechanisms. However, these have been mostly shown to be ineffective in recent clinical trials. Here we tested a novel strategy using a synthetic organic lithium salt, tri-lithium pyrroloquinoline quinonein (Li3PQQ), to modulate mulitple pathways involved in AD pathogenesis. The study of acute toxicity with mice showed Li3PQQ with a very low toxicity (Li3PQQ ID50 5g/kg weight vs. LiCl ID50 2.5g/kg weight). We showed that 8 weeks of daily Li3PQQ administration in the APP/ PS1 mice significantly improved the learning and memory function in the Morris water maze test and facilitated long-term potentiation. Li3PQQ significantly reduced the area and numbers of amyloid plaque and phosphorylated tau levels in cortical areas and mechanistically, it increased activities of Ab-binding alcohol dehydrogenase but decreased activities of glycogen synthase kinase-3 in the transgenic mice. Therefore, Li3PQQ exhibits profound beneficial effects on cognitive impairment and pathological alterations in the AD mouse model. Our study demon- strates the effectiveness of a novel therapeutic strategy for AD through targeting at multiple disease-causing mechanisms. Author details 1Department of Neurology, Zhongshan Hospita

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