About Magtein™:
MAGNESIUM L-THREONATE (Magtein™) is a patented magnesium compound that can help prevent cognitive decline by supporting healthy magnesium levels in the brain. The compound has been shown in extensive preclinical research to enhance recognition memory, spatial working memory, and increase in synaptic density in brain regions critical for memory function. The compound is aimed at treating not just individuals with severe memory loss, but those with trouble concentrating, limited attention spans, and natural memory loss due to aging or neurological diseases. Magnesium Lthreonate will soon undergo clinical studies for use in treating severe memory impairment associated with aging and Alzheimer's Disease.
For more information, please visit: www.magtein.com.
Magtein™ can be purchased from the following websites (among many others):
- http://www.lef.org/Vitamins-Supplements/Item01603/Neuro-Mag-Magnesium-L-Threonate.html
- http://www.swansonvitamins.com/SWU700/ItemDetail
- http://www.walmart.com/ip/B-A-MegaBrain-Dietary-Supplement-Caplets-60ct/19414426
- http://www.rockwellnutrition.com/NeuroMag-capsules-by-Designs-for-Health.html
About Magceutics, Inc.:
Magceutics is a biopharmaceutical company engaged in developing products for improving human memory and learning, and for the treatment of cognitive declines associated with aging, mild cognitive impairment (MCI) and Alzheimer's Disease (AD). The Company's technology is based on the groundbreaking research of Professor Guosong Liu, initiated while he was at the Massachusetts Institute of Technology (MIT). Based on his work in understanding basic neural mechanisms of synaptic density underlying learning and memory, Magceutics was founded to design and develop products for the treatment of memory associated disorders. The Company has identified magnesium l-threonate, a proprietary compound that is safe and, as demonstrated by extensive preclinical testing, highly effective in improving memory functions of healthy rats, aging rats and transgenic AD mice.
Magceutics' approach:
Advances in medicine over the past 20 years have enabled people throughout the developed world to live longer than ever. As a result, the percentage of the population over age 65 is experiencing unprecedented growth, bringing with it a host of new and substantial healthcare challenges. A challenge of particular significance is cognitive decline, a nearly ubiquitous phenomenon of ageing characterized by decreases in language skills, attention, critical thinking, learning, and memory. If the progression of cognitive decline continues, it reaches a disease state known as mild cognitive impairment (MCI) and worse yet, Alzheimer's Disease (AD).
MCI affects 20% of the non-demented population over 65. 60% of patients with MCI go on to develop AD within eight years of diagnosis, at a rate of 10-15% per year. Current estimates of incidence and prevalence for AD in the US alone are staggering: 5.3 million individuals suffer from AD, with 1.3% of the population over 65 newly afflicted each year. More than 26 million are affected worldwide. Despite the massive healthcare challenges MCI and AD present, there is little available to treat the disease. Acetylcholine esterase inhibitors and NMDA antagonists have a disappointingly modest ability to slow AD progression. Nonetheless, despite the limited effectiveness of these drugs, the high prevalence and desperation of AD patients and their families have made them substantial generators of revenue for big pharmaceutical companies ($4 billion/year in the US).
In the quest for a more effective AD treatment, Magceutics has taken an approach fundamentally different from those of our competitors. Thus far, AD drug designs have primarily focused on intervening at various signaling pathways to reduce the production of A-Β in brain, based on the assumption that reducing A-Β should reduce plaque formation, a hallmark of AD. Yet, the real cause of the disease and the causal relationships among the various observed pathological indicators have not been fully established. In fact, the correlation between the severity of the disease and the amount of plaque formation is rather weak (Terry, et al, Ann Neurol, 1991). On the other hand, there is a strong inverse correlation between the number of synapses and the degree of cognitive impairment (Terry, et al, Ann Neurol, 1991; Scheff and Price, Ann Neurol. 1993, Bell et al, J Neurosci, 2007). Therefore, understanding the mechanisms regulating synaptic density is essential for developing an effective therapeutic strategy for prevention of age-dependent memory loss and for treatment of AD.
Professor Liu's lab at MIT conducted extensive research on the regulation of synapse organization with many of the results published in leading journals (Liu & Tsien, Nature, 1995, Tang et al, Nature, 1999, Liu, Nature Neurosci 2004, Wilson et al, J Neurosci, 2007). One of the breakthrough achievements from his lab was the development of a novel functional screening system for identifying compounds capable of increasing synapse density (Slustky et al, Neuron, 2004, Slutsky et al, Neuron, 2010) and establishment of new theory on how to maintain high synaptic density in aging brain. Magceutics used this technique to identify compounds which can increase synapse density and enhance synaptic plasticity.
Research publications:
- The following articles can be downloaded at their respective publication websites:
- Neuron, 2010: Enhancement of Learning and Memory by Elevating Brain Magnesium
- Journal of Neuroscience, 2007: Synaptic Reorganization in Scaled Networks of Controlled Size
- Neuron, 2004: Enhancement of Synaptic Plasticity through Chronically Reduced Ca2 Flux during Uncorrelated Activity
- Nature Neuroscience, 2004: Local Structural Balance and Functional Interaction of Excitatory and Inhibitory Synapses in Hippocampal Dendrites
- Neuron, 2001: A Developmental Switch in Neurotransmitter Flux Enhances Synaptic Efficacy by Affecting AMPA Receptor Activation
- Neuron, 1999: Variability of Neurotransmitter Concentration and Nonsaturation of Postsynaptic AMPA Receptors at Synapses in Hippocampal Cultures and Slices
- Nature, 1995: Properties of Synaptic Transmission at Single Hippocampal Synaptic Boutons