Abstract
Currently, disease-modified strategies to prevent, halt or reverse the progress of Alzheimer’s disease (AD) are still lacking. Previous studies indicated extracts or compounds from Cistanches (ECC) exert a potential neuroprotective effect against AD. Thus, we conducted a preclinical systematic review to assess preclinical evidence and possible mechanisms of ECC in experimental AD. A systematical searching strategy was carried out across seven databases from their inceptions to July 2018. Twenty studies with 1696 rats or mice were involved. Neurobehavioral function indices as primary outcome measures were established by the Morris water maze test (n = 11), step-down test (n = 10), electrical Y-maze test (n = 4), step-through test (n = 3), open field test (n = 2) and passage water maze test (n = 1). Compared with controls, the results of the meta-analysis showed ECC exerted a significant effect in decreasing the escape latency, error times and wrong reaction latency in both the training test and the retention test, and in increasing the exact time and the percentage of time in the platform-quadrant and the number of platform crossings (all P<0.01). In conclusion, ECC exert potential neuroprotective effects in experimental AD, mainly through mechanisms involving antioxidant stress and antiapoptosic effects, inhibiting Aβ deposition and tau protein hyperphosphorylation and promoting synapse protection. Thus, ECC could be a candidate for AD treatment and further clinical trials.
Highlights
Disease-modified strategies to prevent, halt or reverse the progress of Alzheimer’s disease (AD) are still lacking
The prescription drugs approved by the FDA in the US for AD symptom control include: (1) cholinesterase inhibitors (ChEIs) such as donepezil, galantamine, rivastigmine and huperzine A, which maintain average acetylcholine levels by reducing the activity of acetylcholinesterase and (2) N-methyl-Daspartic acid (NMDA) receptor antagonist, memantine, which protects neurons against excessive glutamate by partially blocking NMDA receptors [11]
The evidence available from the present study showed that extracts or compounds from Cistanches (ECC) improved cognitive function in experimental AD mainly through mechanisms involving antioxidant stress and antiapoptosic effects, inhibiting amyloid β (Aβ) deposition and tau protein hyperphosphorylation and promoting synapse protection
Summary
Disease-modified strategies to prevent, halt or reverse the progress of Alzheimer’s disease (AD) are still lacking. Previous studies indicated extracts or compounds from Cistanches (ECC) exert a potential neuroprotective effect against AD. We conducted a preclinical systematic review to assess preclinical evidence and possible mechanisms of ECC in experimental AD. ECC exert potential neuroprotective effects in experimental AD, mainly through mechanisms involving antioxidant stress and antiapoptosic effects, inhibiting Aβ deposition and tau protein hyperphosphorylation and promoting synapse protection. The systematic evaluation of preclinical researches is an essential method to integrate preclinical evidence and can be of high value in improving the quality of preclinical researches and guiding potential clinical translation and application [28, 29]. In the present study, we aim to conduct a preclinical systematic review of the efficacy of ECC and the mechanisms involved in experimental AD
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