Worldwide facing Alzheimer's drug discovery bottlenecks

Sting of Alzheimer’s failures offset by upcoming prevention trials

Nature Reviews Drug Discovery 11:657, 2012

Three prevention trials in asymptomatic Alzheimer’s disease patients will attempt to validate the amyloid hypothesis, evaluate biomarkers and set the stage for drug approvals.

Alzheimer’s disease, Dementia, is commonly known as Senile dementia. Early phase of Alzheimer’s also known as mild cognitive impairment. Its early symptoms of learning and memory impairment allow physicians to diagnose the disease. As the disease progresses to mid-term, patients will lose independence and become unable to carry out daily activities. During the final stage of Alzheimer's disease, the patient is completely dependent on caregivers. According to many surveys, 15% of people over the age of 80 are suffering from dementia. Once we begin to consciously take notice of our forgetfulness, the inevitable effects of aging have already begun, and healthy longevity with optimal mental function should be our ultimate goal.

       As of  2012, more than 1000 clinical trials have been performed studying how to treat Alzheimer’s, however, it is still unknown whether this research found any method of treatment that are truly effective. Even prominent persons such as former United States President Ronald Reagan and the former United Kingdom's Prime Minister Margaret Thatcher, both of whom had access to the best medical care, were still unable to escape death from Alzheimer's. Therefore, the existing medication has shown limited effectiveness in the long term.  

In Western medicine, drug development usually focuses on inhibition rationale, for example, anti-cancer drugs are designed to inhibit the growth of cancer cells, but whether these drugs will kill the faster growing bone marrow stem cells really depend on fortune of the patients.

Alzheimer’s drug development is no exception. Currently, the two clinical treatments are acetylcholine enzyme inhibitors or NMDA receptor inhibitors. Acetylcholine enzyme inhibitors focus on inhibition of the enzyme acetylcholinesterase which breaks down acetylcholine, a neurotransmitter required for memory function. NMDA receptor inhibitors were developed to address an excess of the nerve conduction factor glutamate which binds the NMDA receptors on brain cells. NMDA receptors are the predominant molecular device for controlling synaptic plasticity and memory function. The suppression philosophy of new drug development for the last 60 years has not proven satisfactory, and yet this philosophy continues.  This has created a bottleneck in Western drug development. The failure of the last two inhibitory monoclonal antibody drugs in clinical phase III left these big international pharmaceutical companies, Pfizer, Johnson & Johnson (J&J) and Elan, not knowing how to proceed further. In an attempt to move beyond these disappointing results, researchers both inside these pharmaceutical companies and in independent laboratories have now turned to development of preventive drug rather than therapeutic drugs for Alzheimer’s disease. They barely hope that treating patients with no symptoms or early onset symptoms might give them better chance for success in Alzheimer’s drug development.

      The AcaMed company’s R&D team used the electronic database containing 700 kinds of ancient traditional Chinese medicine books and found that reishi is one of the few herbs that were recorded to have the effect on enhancing intelligence. After many years of research , we found that the extract and the purified compounds from reishi can induce glial cells for nerve growth factor production, and this nerve growth factor has the ability to remove the accumulation of abnormal aggregates of the neuronal cells, thus allowing our neurons to resume long-term memory function. Our company’s R&D team has published this study in the world famous journal “Neuropharmacology (2012)”. In addition, we discovered that shouwu and huangjing concentrates will induce neurons to produce erythropoietin and to promote energy generation of mitochondria. Further studies showed considerable improvement in experimental animal models of Alzheimer's disease and neuronal injury.

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