To assess the efficacy of the Ginkgo biloba in patients with dementia of the Alzheimer type in slowing down the disease's degenerative progression and the patients' cognitive impairment compared with rivastigmine.
Total 56 patients aged 50-75 years, suffering from dementia, were allocated into one of the two treatments: group 1) Ginkgo biloba (120 mg daily dose); group 2) rivastigmine (4.5 mg daily dose) in a 24-week randomized double blind study. The degree of severity of dementia was assessed by the Seven Minute test and the Mini-Mental State Examination.
Our results confirm the clinical efficacy of rivastigmine in the dementia of the Alzheimer type, comparing to Ginkgo biloba. There are few published trials that have directly compared a cholinesterase inhibitor with Ginkgo for dementia. This study directly compares a cholinesterase inhibitor with Ginkgo biloba for dementia of the Alzheimer type.
Our study suggests that there are differences in the efficacy of Ginkgo biloba and rivastigmine in the treatment of Alzheimer's dementia. In addition, this study suggested that cholinesterase inhibitors should be used in preference to Ginkgo biloba in patients with mild to moderate AD.
[Show abstract][Hide abstract] ABSTRACT: Alzheimer’s disease (AD) is a neurodegenerative disorder that is characterized by normal memory loss and cognitive impairment in humans. Many drug targets and disease-modulating therapies are available for treatment of AD, but none of these are effective enough in reducing problems associated with recognition and memory. Potential drug targets so far reported for AD are β-secretase, Γ-secretase, amyloid beta (Aβ) and Aβ fibrils, glycogen synthase kinase-3 (GSK-3), acyl-coenzyme A: cholesterol acyl-transferase (ACAT) and acetylcholinesterase (AChE). Herbal remedies (antioxidants) and natural metal-chelators have shown a very significant role in reducing the risk of AD, as well as lowering the effect of Aβ in AD patients. Researchers are working in the direction of antisense and stem cell-based therapies for a cure for AD, which mainly depends on the clearance of misfolded protein deposits — including Aβ, tau, and alpha-synuclein. Computational approaches for inhibitor designing, interaction analysis, principal descriptors and an absorption, distribution, metabolism, excretion and toxicity (ADMET) study could speed up the process of drug development with higher efficacy and less chance of failure. This paper reviews the known drugs, drug targets, and existing and future therapies for the treatment of AD.
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