Abstract
Alzheimer’s disease (AD) is the most common cognitive disorder in the elderly population. However, effective pharmacological agents targeting AD have not been developed. The processed Polygoni multiflori Radix (PPM) and its main active substance, 2,3,5,4′-tetrahydroxystilbene-2-O-β-glucoside (TSG), has received considerable attention, majorly due to its neuroprotective activities against multiple biological activities within the human body. In this study, we provide new evidence on the therapeutic effect of PPM and TSG during cognitive impairment by evaluating the ameliorative potential of PPM and TSG in scopolamine-induced amnesia in ICR mice. PPM (100 or 200 mg/kg) was orally administered during the experimental period (days 1–15), and scopolamine was intraperitoneally injected to induce cognitive deficits during the behavioural test periods (days 8–15). The administration of PPM and TSG significantly improved memory loss and cognitive dysfunction in behavioural tests and regulated the cholinergic function, brain-derived neurotrophic factor, and neural apoptosis. The present study suggests that PPM and TSG improved scopolamine-induced cognitive dysfunction, but further study has to be supported for the clinical application of PPM and TSG for AD prevention and treatment.
Highlights
With the increase in the ageing population, the number of people living with dementia has been increasing
This study aimed to investigate the improvement effect of processed Polygoni multiflori Radix (PPM) and its major substance, TSG, on cognitive impairment using novel object recognition (NOR), passive avoidance (PA), and Morris water maze (MWM)
The results of the present study showed that neuronal apoptosis, as indicated by the ratio of Bcl-2-associated X (Bax) to B-cell lymphoma 2 (Bcl-2) expression in the brain, was significantly increased in the scopolamine-injected control group compared with the normal group
Summary
With the increase in the ageing population, the number of people living with dementia has been increasing. In 2015, the number of people living with dementia was estimated to be 46.8 million worldwide, which is estimated to rise to 74.7 million in 2050 [1]. In AD, there is a cerebral accumulation of plaque deposits of the β-amyloid peptide (Aβ) and tau protein aggregation into neurofibrillary tangles [3]. Another characteristic feature of AD is reduced production of certain brain chemicals necessary for communication between nerve cells, such as acetylcholine (ACh), norepinephrine, serotonin, and somatostatin [4]
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