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Can Alzheimer be reversed? Scientists make a great discovery!

2017-02-06 来源:转载自第三方
6 February 2017
  Recently, Japanese scientists published a paper in the journal Neuropharmacology entitled "Pharmacological Properties of SAK3, a Novel T-type Voltage-gated Ca2+ Channel Enhancer", they found a drug called SAK3, which can improve Cav3.1 and Cav3.3T-type Ca2+ channel currents, promote the release of ACh in the hippocampus, it may be able to effectively treat Alzheimer's disease.
  Alzheimer is a primary neuronal degeneration-based neurodegenerative disorder that occurs during presenium and senectitude. According to the World Health Organization, there are more than 47 million dementia patients, of which 60% live in low- and middle-income countries. Affected by the aging population, this figure is expected to triple by 2050. Dementia and cognitive disorders have been the leading contributors to chronic disease in the world, leading to disability and dependence on older persons. Etiology and pathogenesis of Alzheimer's disease is not clear. It is generally believed that Alzheimer's disease is associated with many factors such as inheritance, aging, immune function abnormality, sex hormone level, environment and so on. Various hypotheses are proposed, including cholinergic hypothesis, Aβ abnormal deposition hypothesis, Tau protein hypothesis, free radical Injury hypothesis, calcium homeostasis hypothesis, glutamate excitatory hypothesis and gene mutation hypothesis.
  In the anti-Alzheimer's drug, there are ten categories, cholinesterase inhibitors, anti-amyloid β protein, anti-tau protein phosphorylation, antioxidant stress, anti-apoptosis, NMDA Receptor antagonists, synergistic synergism, anti-inflammatory effects, neurotropic metabolites, and neural stem cell transplantation.
  Acetylcholine is a neurotransmitter in the brain, and has a close relationship with memory, can slow down the rate of memory loss. Because of the restoration of benign amnesia and effective prevention of Alzheimer's disease, it is called as the body's "memory Element" by nerve biologists. The body's acetylcholine system imbalance is considered to be one of the reasons which induce Alzheimer's disease and vascular dementia. The researchers found that SAK3, a T-type channel enhancer, stimulates the release of acetylcholine in the brain by activating the memory molecule CaMKII, and improves the cognitive function of the brain. SAK3 also reduces beta-amyloid production in the mouse model, it also may be able to help researchers develop the first disease-modifying drugs to prevent mild to moderate Alzheimer's disease. Animal experiments show that the drug has a certain safety and tolerance, the researchers hope to be able to take clinical trials in the next few years to prove the effectiveness of the drug.
  In fact, over the years, the researchers never give up the research and exploration for treatment of Alzheimer's disease. As early as 2011, there are scientists through chemical methods to prepare for 2-aminothiazole derivatives, which is for treatment and prevention of Alzheimer's disease, the drug has the right molecular weight, structural stability, it can penetrate the cell membrane, has little toxic side effects and other advantages; a research team from the University of Minnesota also published research results in the journal "Nature Medicine" recently. They restored the learning and memory deficits of mice to a certain extent by blocking the "caspase-2" The specific enzyme activity. The enzyme "caspase-2" may be a new therapeutic target for Alzheimer, some cognitive impairment caused by "tau disease" can be reversed by blocking "caspase-2" function.
  Although the anti-Alzheimer's drugs are few, but scientists are fully committed to do the research. We firmly believe that as long as we have to pay attention to Alzheimer's disease research, we can develop a cure in the future, so as to effectively improve the living quality of patients.
Related link: 2-Aminothiazole
                     Summaries of Researches on Alzheimer's Disease (AD) Last Year
Edited by the Editorial Office of Suzhou Yacoo Science Co., Ltd.


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