Memogain is a pro-drug of galantamine (Reminyl®, Razadyne®), which has been marketed around the world for over 15 years for symptomatic AD treatment. Intranasal administration of the pro-drug achieves higher dose levels in the brain while avoiding the compliance-impairing gastro-intestinal adverse effects of existing drugs, such as Aricept® and Exelon®.
Memogain has a unique mechanism of action:
- It enhances the responsiveness of nicotinic receptors, including the alpha-7 subtype, to acetylcholine and choline, without additional desensitization. Nicotinic receptors are recognised as important drug targets for improving cognition and behavior and enhancing neuronal survival. Memogain’s allosteric modulatory effect on nicotinic receptors is completely different from that of ‘PAMs’ (positive allosteric modulators). PAMs mainly act on desensitized receptors and after initial re-activation lead to further inactivation by desensitization. In contrast, Memogain acts by way of a natural mechanism of up-regulation of nicotinic receptors, in addition to being a cholinesterase inhibitor, as are other approved AD drugs.
- Memogain also has the potential to slow or inhibit disease progression. In transgenic animal models of AD, Memogain has been shown to dramatically reduce the amyloid plaque burden typical for AD. In other models, the drug has induced neurogenesis in areas of Alzheimer-caused neurodegeneration, such as the hippocampus, as well as functional migration and phenotypic maturation of newly produced neurons. Both, reduced plaque formation and neurogenesis, are evidence of disease modification, the ultimate goal of AD drug development. Studies are planned to test whether the disease-modifying effects seen in animal studies translate to humans.
Memogain may also offer medical benefit to patients of Parkinson’s disease and other neurodegenerative diseases.