Efficacy and safety of Ginkgo biloba extract EGb 761 in mild cognitive impairment with neuropsychiatric symptoms: a randomized, placebo-controlled, double-blind, multi-center trial.

OBJECTIVE: The study was conducted to explore the effects of EGb 761 (Dr. Willmar Schwabe GmbH & Co. KG, Karlsruhe, Germany) on neuropsychiatric symptoms (NPS) and cognition in patients with mild cognitive impairment (MCI). METHODS: One hundred and sixty patients with MCI who scored at least 6 on the 12-item Neuropsychiatric Inventory (NPI) were enrolled in this double-blind, multi-center trial and randomized to receive 240 mg EGb 761 daily or placebo for a period of 24 weeks. Effects on NPS were assessed using the NPI, the state sub-score of the State-Trait Anxiety Inventory and the Geriatric Depression Scale. Further outcome measures were the Trail-Making Test (A/B) for cognition and global ratings of change. Statistical analyses followed the intention-to-treat principle. RESULTS: The NPI composite score decreased by 7.0 ± 4.5 (mean, standard deviation) points in the EGb 761-treated group and by 5.5 ± 5.2 in the placebo group (p = 0.001). Improvement by at least 4 points was found in 78.8% of patients treated with EGb 761 and in 55.7% of those receiving placebo (p = 0.002). Superiority of EGb 761 over placebo (p < 0.05) was also found for the State-Trait Anxiety Inventory score, the informants' global impression of change, and both Trail-Making Test scores. There were statistical trends favoring EGb 761 in the Geriatric Depression Scale and the patients' global impression of change. Adverse events (all non-serious) were reported by 37 patients taking EGb 761 and 36 patients receiving placebo. CONCLUSIONS: EGb 761 improved NPS and cognitive performance in patients with MCI. The drug was safe and well tolerated.

[Experience in clinical use of tanakan in the treatment of the syndrome of mild cognitive impairment].

Clinical efficacy and safety of tanakan has been studied in 30 patients with the syndrome of mild cognitive impairment. The results suggest a clear therapeutic effect of the 6 month course therapy. The efficacy of tanakan was confirmed by significant improvement of cognitive functioning of patients measured with MMSE, MDRS, FAST and other scales. The feature of tanakan effect is its positive influence on memory and other cognitive functions that allows the use of the drug in the treatment of elderly people with the syndrome of mild cognitive impairment. The safety of tanakan used in high therapeutic dosages (240 mg daily) and its good tolerability during chronic administration are revealed.

[Tanakan (EGb 761) in the therapy of mild cognitive impairment].

Mild Cognitive Impairment (MCI) means cognitive deterioration not yet causing disability or dementia. Aged patients with MCI constitute a group of high risk for Alzheimer disease and other types of dementia. Currently, there is no generally adopted approach to MCI management but medications with neuroprotective properties are presumed to be the most perspective. Presented are the results of a multicentral open-label clinical trial of vascular and neuroprotective drug tanakan (EGb 761). The study has shown the decrease of cognitive impairment, which was both clinically and statistically significant, in patients at early stages of vascular and neurodegenerative pathological process. Probable efficacy of long-term tanakan treatment in prevention of dementia is discussed.

[Current strategies of pathogenetic therapy of Alzheimer's disease]. / Sovremennye strategii patogeneticheskoi terapii bolezni Al'tsgeimera.

This is a review of the data available in the literature and the authors' own findings on pathogenetical rationale for the use and clinical study of current treatments for Alzheimer's disease (AD) (synonym: Alzheimer-type dementia). In the past decade many attempts have been made at targeting different links of the pathogenesis of a neurodegenerative process that underlie AD. Several areas of pathogenetical therapy for AD have been developed on the basis of experimental studies and pilot clinical tests. The most developed areas are as follows: various compensatory (replacement) treatments aimed at overcoming neurotransmitter deficit in different neuronal systems that are damaged in AD to a greater or lesser extent; neuroprotective therapy promoting increased viability (survival) of neurons and their plasticity, and vasoactive therapy. Rather new directions of AD pathogenetic therapy, such as antiinflammatory and hormonal therapy along with antiamyloid therapeutic strategies are still under study.