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Curr Med Sci ; 40(1): 18-27, 2020 Feb.
Article in English | MEDLINE | ID: mdl-32166661

ABSTRACT

Alzheimer's disease (AD) shows cognitive impairments in clinic, which is multifactorial with different etiopathogenic mechanisms such as Aß deposition, neuroinflammation and neuronal dystrophy involved. Therefore, multi-targets drugs with neuroprotective, anti-amyloidogenic and anti-inflammatory properties will be effective in AD treatment. Epigallocatechin-3-gallate (EGCG) possesses a broad spectrum of pharmacological activities in the prevention and treatment of multiple neurodegenerative diseases. In the present study, we showed that oral administration of EGCG (50 mg/kg) for 4 months significantly attenuated the cognitive deficits in APP/PS1 transgenic mice, which served as AD model. Moreover, EGCG induced an improvement in dendritic integrity and expression levels of synaptic proteins in the brain of APP/PS1 mice. And EGCG exerted obvious anti-inflammatory effects, which was manifested by alleviating microglia activation, decreasing pro-inflammatory cytokine (IL-1ß) and increasing anti-inflammatory cytokines (IL-10, IL-13). Furthermore, ß-amyloid (Aß) plaques were markedly reduced in the hippocampus of 6-month old APP/PS1 mice after EGCG treatment. In conclusion, these findings indicate that EGCG improves AD-like cognitive impairments through neuroprotective, anti-amyloidogenic and anti-inflammatory effects, thus is a promising therapeutic candidate for AD.


Subject(s)
Alzheimer Disease/psychology , Amyloid beta-Protein Precursor/genetics , Catechin/analogs & derivatives , Cognitive Dysfunction/drug therapy , Neuroprotective Agents/administration & dosage , Presenilin-1/genetics , Administration, Oral , Alzheimer Disease/drug therapy , Alzheimer Disease/genetics , Amyloid beta-Protein Precursor/metabolism , Animals , Catechin/administration & dosage , Catechin/pharmacology , Cognitive Dysfunction/etiology , Cognitive Dysfunction/metabolism , Cytokines/metabolism , Disease Models, Animal , Gene Expression Regulation , Humans , Mice , Mice, Transgenic , Mutation , Neuroprotective Agents/pharmacology , Treatment Outcome
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