Glucose metabolism plays a significant role in the central nervous system. Unlike other organs, the brain depends entirely on the energy provided by glucose metabolism for neuronal activity, and an insufficient supply of blood glucose can cause neurological damage[1-2]. The level of glucose metabolism is closely associated with cerebrovascular disease, amyloid β production and clearance, and Tau phosphorylation, indicating that abnormal glucose metabolism is closely related to the pathogenesis of Alzheimer's disease (AD)[3-5]. Zensun has therefore proposed a new strategy to improve brain energy metabolism in order to prevent and treat AD. We have generated ZS-07 as a multi-component synergistic combination of new therapeutic drugs affecting a variety of targets of brain energy metabolism.
Preclinical studies have shown that ZS-07 is a potential candidate for the treatment of AD., as it improves memory and autonomic activity, and decreases anxiety in animal models. ZS-07 is a safe compound preparation patented by Zensun (patent no. CN201710131111.X). The safety of various components of ZS-07 has been demonstrated over years of medical practice.
About Alzheimer’s Disease
Alzheimer`s disease (AD) is most frequently found in people over the age of 65. AD is a chronic neurodegenerative disease that has a progressive pattern of cognitive and functional impairment, and is the most common cause of dementia.
In 2015, there were approximately 48 million AD patients in the world, and this number has been growing by about 7.7 million every year. It is estimated that in 2050 there will be 135 million AD patients in the world. The United States spent $236 billion in 2016 on treating and caring for AD patients.
Currently, there is a lack of effective treatment and preventive measures for Alzheimer's disease. Five AD drugs were approved by the FDA ten years ago--Tacrine, Donepezil, Rivastigmine, Galantamine, and Memantine. The combination therapy of memantine /donepezil was approved in 2014. These approved AD drugs are classified in two categories--acetylcholinesterase inhibitors and NMDA receptor antagonists. Unfortunately, although designed to slow down the decline and loss of cognitive function by changing brain neurotransmitter activities in AD patients, these drugs only delay the worsening of symptoms for about 6-12 months, and often have severe side effects. It is important to develop therapeutically significant drugs with a better safety profile that can block or reverse the course of AD.
Dienel, G. A. Chapter 3 - Energy Metabolism in the Brain. From Molecules to Networks (Third Edition). Boston, 2014, Academic Press: 53-117.
Mohseni, S. Chapter 33 - Neurologic damage in hypoglycemia. Handbook of Clinical Neurology. W. Z. Douglas and A. M. Rayaz, Elsevier. 2014, 126: 513-532.
Baker L D, Cross D, Minoshima S, et al. Insulin resistance and Alzheimer-like reductions in regional cerebral glucose metabolism for cognitively normal adults with prediabetes or early type 2 diabetes.[J]. JAMA Neurology, 2011, 68(1): 51-57.
O'Connor T, Sadleir K R, Maus E, et al. Phosphorylation of the translation initiation factor eIF2α increases BACE1 levels and promotes amyloidogenesis[J]. Neuron, 2008, 60(6): 988-1009.
 Whitmer R A, Karter A J, Yaffe K, et al. Hypoglycemic episodes and risk of dementia in older patients with type 2 diabetes mellitus[J]. Jama, 2009, 301(15): 1565-1572.