ABSTRACT
Alzheimer's disease (AD) is a common neurodegenerative disease in the elderly individuals and its effective therapies are still unavailable. This study was designed to investigate the neuroprotection of sulforaphane (SFN) in AD-lesion mice induced by combined administration of d-galactose and aluminium. Results showed that SFN ameliorated spatial cognitive impairment and locomotor activity decrease in Morris water maze and open field test, respectively. And attenuated numbers of amyloid ß (Aß) plaques in both hippocampus and cerebral cortex of AD-lesion mice were detected by immunohistochemistry. According to spectrophotometry and quantitative reverse-transcriptase polymerase chain reaction results, a significant increase in carbonyl group level and obvious decreases in both activity and messenger RNA expression of glutathione peroxidase were found in brain of AD-lesion mice compared with control, but not in SFN-treated AD-lesion mice. In conclusion, SFN ameliorates neurobehavioral deficits and protects the brain from Aß deposits and peroxidation in mice with Alzheimer-like lesions, suggesting SFN is likely a potential phytochemical to be used in AD therapeutics.
Subject(s)
Alzheimer Disease/drug therapy , Amyloid beta-Peptides/drug effects , Behavior, Animal/drug effects , Cerebral Cortex/drug effects , Isothiocyanates/pharmacology , Neuroprotective Agents/pharmacology , Oxidative Stress/drug effects , Plaque, Amyloid/drug therapy , Alzheimer Disease/prevention & control , Amyloid beta-Peptides/metabolism , Animals , Cerebral Cortex/metabolism , Disease Models, Animal , Female , Hippocampus/drug effects , Hippocampus/metabolism , Male , Mice , Mice, Inbred C57BL , Oxidative Stress/physiology , Plaque, Amyloid/metabolism , Random Allocation , SulfoxidesABSTRACT
The objective of our study was to perform an updated meta-analysis of placebo-controlled RCTs of Huperzine A (Hup A) on patients with Alzheimer's disease (AD) and vascular dementia (VD), in order to provide the basis and reference for clinical rational drug use. The primary outcome measures assessed were minimental state examination (MMSE) and activities of daily living scale (ADL). Eight AD trials with 733 participants and two VD trials with 92 participants that met our inclusion criteria were identified. The results showed that Hup A could significantly improve the MMSE and ADL score of AD and VD patients, and longer durations would result in better efficacy for the patients with AD. It seemed that there was significant improvement of cognitive function measured by memory quotient (MQ) in patients with AD. Most adverse effects in AD were generally of mild to moderate severity and transient. Compared to the patients with AD, Hup A may offer fewer side effects for participants with VD in this study. Therefore, Hup A is a well-tolerated drug that could significantly improve cognitive performance in patients with AD or VD, but we need to use it with caution in the clinical treatment.