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Alzheimer's disease (AD) is a complex neurodegenerative disease affecting mental ability and neurocognitive functions. Crinum woodrowii Baker (C. woodrowii) is an endemic plant with significant ethnobotanical potential against neurological and inflammatory conditions with a characteristic improvement of cognitive functions.To assess the anti-AD potential of C. woodrowii extract through in-vitro assays and preclinical in-vivo screening and to validate its neuroprotective effect by biochemical and histopathological analysis.Herein, galantamine contents of the ethanolic extract of C. woodrowii were quantified using HPLC and LCMS. Further, the extract was examined for in-vitro cytotoxicity, anti-inflammatory, anti-cholinesterase activities, and in-vivo neuropharmacological studies.The extract exhibited low cytotoxicity on RAW 264.7 cells and the inhibition of LPS-induced nitric oxide production. The extract also showed anti-cholinesterase activities. The treatment with extract significantly rescued the rough eye phenotype in the Drosophila model of AD. In neuropharmacological screening, the extract showed no symptoms of acute oral toxicity in rats. The extract significantly reversed scopolamine-induced memory deficit in mice and improved their learning ability with memory retention in exteroceptive behavioral models. The pretreatment of mice with extract reinstated the elevated brain acetylcholinesterase, lipid peroxidation, and reduced glutathione levels due to scopolamine and aging. The extract also restored the altered superoxide dismutase and catalase levels. The extract alleviated neuronal tissue damage caused by the scopolamine, as indicated by the histological analyses of the brain.Our findings suggested that the C. woodrowii extract has neuroprotective properties and ameliorates cognitive dysfunction and hence could be explored further as a potential neurotherapeutics for treating AD.

PurposeThis study aimed to validate the accuracy of the Active Style Pro HJA-750C (ASP) in measuring metabolic equivalents (METs) during walking and reaching tasks in individuals with subacute stroke using a respiratory gas analyzer as a reference.MethodsTwenty-three hospitalized patients with subacute stroke participated in this study. They performed sitting and standing reaching tasks, as well as walking while wearing a VO2 Master respiratory gas analyzer and ASP devices on both the paretic and non-paretic sides. The METs values recorded by the ASP were compared with those obtained using a VO2 Master respiratory gas analyzer. Pearson's correlation coefficients were calculated for each task, and Bland–Altman plots were used to assess the agreement between the two methods.ResultsThe ASP demonstrated good concurrent validity, with correlation coefficients of 0.71 and 0.74 for the sitting reaching task, 0.75 and 0.79 for the standing reaching task, and 0.83 and 0.85 for walking when the ASP was placed on the paretic and non-paretic sides, respectively. Bland–Altman analysis indicated no significant fixed or proportional errors. The ASP accurately measures METs whether worn on the affected or unaffected side of the waist.ConclusionThe ASP provides valid measurements of physical activity during walking and reaching tasks in patients with subacute stroke. These findings suggest that ASP is a valuable tool for monitoring physical activity in clinical rehabilitation settings.

A moderate amount of ethanol (EtOH) intake can lower the incidence of various cardiovascular disease but can result in neuropsychiatric issues during adolescence. EtOH acts on GABAA receptor, which can slow down neurotransmission and lead to changes in synaptic functions. These neurological changes due to EtOH can result in transient memory loss and may increase the risk of developing various neurological and psychiatric disorders such as dementia. Therefore, there is a need for strategies to overcome EtOH-induced brain dysfunctions. In this study, we investigated the effects of oleanolic acid (OA) on EtOH-induced memory impairment. OA blocked functional impairment of N-methyl-D-aspartate receptors (NMDAR), which are a key mechanism in EtOH-induced memory impairments. OA inhibited the removal of the major subunit of NMDAR, NR2a, from synapses induced by EtOH. Based on this, OA inhibited the impairment of object recognition memory caused by EtOH. Although OA failed to modulate the blood alcohol and acetaldehyde levels in EtOH-treated mice, OA blocked EtOH-induced increase in brain allopregnalone level with reducing 5α-reductase level. These results indicate that OA inhibits EtOH-induced memory impairment by regulating NMDAR function and passably modulates neurosteroid system.