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Background: Effective interventions for overall healthy subjects with mild cognitive impairment are currently limited. Choline alphoscerate (alpha glyceryl phosphorylcholine, αGPC) is a choline-containing phospholipid used to treat cognitive function impairments in specific neurological conditions. This study aimed to investigate the efficacy and safety of αGPC in individuals diagnosed with mild cognitive impairment. Methods: In this multicenter, randomized, placebo-controlled trial, 100 study subjects with mild cognitive impairment underwent a double-blind SHCog™ soft capsule (600 mg αGPC) or placebo treatment for 12 weeks. The primary efficacy outcome included changes from baseline on the Alzheimer's Disease Assessment Scale–cognitive subscale (ADAS-cog). Safety assessments included regular monitoring of adverse events, and clinical laboratory tests were conducted at baseline and the end of the trial. Results: After 12 weeks of αGPC treatment, the ADAS-cog score decreased by 2.34 points, which was significantly greater than the change observed in the placebo group. No serious AEs were reported, and no study subjects discontinued the intervention because of AEs. There was no significant difference in incidence rate of AEs between the αGPC group and the placebo group. Conclusion: This study suggests that αGPC is a safe and effective intervention for improving cognitive function in study subjects with mild cognitive impairment. Trial registration: Clinical Research Information Service; Osong (Chungcheongbuk-do): Korea Centers for Disease Control and Prevention, Ministry of Health and Welfare (Republic of Korea); KCT0008797; A 12-week, multicenter, randomized, double-blind, placebo-controlled human application study to evaluate the efficacy and safety of SH_CAPK08 on cognitive function improvement in mild cognitive decline. [ABSTRACT FROM AUTHOR]

The clinical benefits of nootropics in the treatment of cognitive decline has been either limited or controversial. This study aimed to observe the effectiveness of cholinesterase inhibitor (ChEI) and nootropics combination in the treatment of cognitive impairment in dementia. Data were based on electronic medical records in a university health system. Patients with mild-to-moderate dementia and no history of prior cognitive enhancer use were included (n = 583). The subjects were categorized into the ChEI only group and the ChEI and nootropics combination group. The primary outcome measure was the change in cognitive function, as assessed by the mini-mental state examination (MMSE) from baseline to 300–400 days after the first ChEI prescription. Subsequent analyses were conducted in consideration of the dementia type, medical adherence, and type of nootropics. The changes in MMSE scores from baseline to endpoint were not significantly different between the two groups. In Alzheimer's dementia, the combination group showed significantly less deterioration in MMSE language subscale scores compared to the ChEI only group (F = 6.86, p = 0.009), and the difference was consistent in the highly adherent subjects (F = 10.16, p = 0.002). The choline alfoscerate and the ginkgo biloba extract subgroups in Alzheimer's dementia showed more significant improvements in the MMSE language subscale scores compared to the other nootropics subgroup (F = 7.04, p = 0.001). The present study showed that the effectiveness of ChEI and nootropics combination on cognition may appear differently according to the dementia type. This emphasizes the need for well-controlled studies to generalize the effectiveness of nootropics across various clinical settings. [ABSTRACT FROM AUTHOR]

The early identification and prevention of dementia is important for reducing its worldwide burden and increasing individuals’ quality of life. Although several dementia prediction models have been developed, there remains a need for a practical and precise model targeted to middle-aged and Asian populations. Here, we used national Korean health examination data from adults (331,126 individuals, 40–69 years of age, mean age: 52 years) from 2002–2003 to predict the incidence of dementia after 10 years. We divided the dataset into two cohorts to develop and validate of our prediction model. Cox proportional hazards models were used to construct dementia prediction models for the total group and sex-specific subgroups. Receiver operating characteristics curves, C-statistics, calibration plots, and cumulative hazards were used to validate model performance. Discriminative accuracy as measured by C-statistics was 0.81 in the total group (95% confidence interval (CI) = 0.81 to 0.82), 0.81 in the male subgroup (CI = 0.80 to 0.82), and 0.81 in the female subgroup (CI = 0.80 to 0.82). Significant risk factors for dementia in the total group were age; female sex; underweight; current hypertension; comorbid psychiatric or neurological disorder; past medical history of cardiovascular disease, diabetes mellitus, or hypertension; current smoking; and no exercise. All identified risk factors were statistically significant in the sex-specific subgroups except for low body weight and current hypertension in the female subgroup. These results suggest that public health examination data can be effectively used to predict dementia and facilitate the early identification of dementia within a middle-aged Asian population. [ABSTRACT FROM AUTHOR]

Mild cognitive impairment is a typical symptom of early Alzheimer's disease (AD). Glehnia littoralis (G. littoralis), a medicinal halophyte plant commonly used to treat strokes, has been shown to possess some therapeutic qualities. In this study, we investigated the neuroprotective and anti-neuroinflammatory effects of a 50% ethanol extract of G. littoralis (GLE) on lipopolysccharide (LPS)-stimulated BV-2 cells and scopolamine-induced amnesic mice. In the in vitro study, GLE treatment (100, 200, and 400 µg/mL) markedly attenuated the translocation of NF-κB to the nucleus concomitantly with the significant mitigation of the LPS-induced production of inflammatory mediators, including NO, iNOS, COX-2, IL-6, and TNF-α. In addition, the GLE treatment suppressed the phosphorylation of MAPK signaling in the LPS-stimulated BV-2 cells. In the in vivo study, mice were orally administered with the GLE (50, 100, and 200 mg/kg) for 14 days, and cognitive loss was induced via the intraperitoneal injection of scopolamine (1 mg/kg) from 8 to 14 days. We found that GLE treatment ameliorated memory impairment and simultaneously improved memory function in the scopolamine-induced amnesic mice. Correspondingly, GLE treatment significantly decreased the AChE level and upregulated the protein expression of neuroprotective markers, such as BDNF and CREB, as well as Nrf2/HO-1 and decreased the levels of iNOS and COX-2 in the hippocampus and cortex. Furthermore, GLE treatment attenuated the increased phosphorylation of NF-κB/MAPK signaling in the hippocampus and cortex. These results suggest that GLE has a potential neuroprotective activity that may ameliorate learning and memory impairment by regulating AChE activity, promoting CREB/BDNF signaling, and inhibiting NF-κB/MAPK signaling and neuroinflammation. [Display omitted] • GLE can inhibit the over activation of BV-2 cells by reducing the release of NO and inflammatory factors. • GLE can play an anti-inflammatory role through MAPK/NF-κB signaling pathways induced by LPS. • GLE reversed memory impairment through enhancing BDNF/CREB expression in scopolamine-induced C57BL/6 mouse model. • GLE prevents oxidative stress by regulating Nrf-2/HO-1 expression in scopolamine-induced C57BL/6 mouse model. [ABSTRACT FROM AUTHOR]