A study led by scientists at the Hong Kong University of Science and Technology and the University of Glasgow, UK found that a protein called IL-33 can reverse the symptoms and decrease of cognitive function for mice with Alzheimer's disease. The study was published in the Journal PNAS on April 18th.
Professor Nancy Y Ip at Chinese Academy of Sciences and Hong Kong University of Science and Technology and Professor Eddy Liew at Infection, Immunology and Inflammation Research Institute of University of Glasgow are the co-leaders of the study. Professor Nancy Y Ip mainly studies on relationship between neurotrophic factor and neuronal development.
Functional integrity of the cerebral neocortex, dependent on the correct amount of excitatory neurons and inhibitory neurons. But it is not clear, new abnormal cortical neurons during the development of production will lead to consequences. Nancy Ip research team found that neurons in the neocortex upper overproduction will lead to similar autistic behavior. They then confirmed, S- nitrosylation (S-nitrosylation) proteasome-dependent degradation of p35 inhibits Cdk5 activity, regulation of hippocampal synaptic strength. The findings published on Nature Communications magazine.
Alzheimer's disease is a devastating disease, and there is no effective treatment currently. It is the most common cause of dementia in the UK affects about 85 million people mostly aged 65 or older. It affects people between the ages of 1/14 with the positive growth of our aging population. It is estimated that there will be 65 million people worldwide suffering from Alzheimer's disease till 2030.
Professor Eddy Liew said, "Alzheimer's disease is currently in urgent unmet clinical needs. We hope that our findings may ultimately translate to humans. Organism in various cell types can be produced by IL-33, the protein in particularly abundant in the central nervous system (brain and spinal cord) in. we formed a mouse strain progressive disease like Alzheimer's disease (APP / PS1) of age to carry out experiments. we found that injection of IL-33 to senescence APP / PS1 mice, can rapidly improve their memory and cognitive function in a week to normal levels in mice of the same age."
Some signs of Alzheimer's disease include the presence of extracellular deposits of amyloid protein plaques, neurofibrillary tangles in the brain is formed. In the course of the disease, 'plaques' and 'tangles' accumulation, leading to the loss of connections between nerve cells, eventually neuronal cell death, loss of brain tissue.
IL-33 appears to be to work through the mobilization of microglial cells surrounding the amyloid plaques, absorb and digest them, to reduce the number and size of plaques. IL-33 is a known degradable soluble amyloid by inducing enzyme neprilysin to do this. In addition, IL-33 therapy may be acting by inhibiting inflammation of the brain tissue, the researchers confirmed earlier inflammation promotes the formation of plaques and tangles. Thus, IL-33 not only helps clear amyloid plaques have formed, but also the first stop of the plaques and tangles deposition.
Professor Liew added, "is not clear that the current findings associated with human Alzheimer's disease, but there are some encouraging clues. For example, some previous studies confirmed the genetic mutation of IL-33 in Europe and China the association between Alzheimer's disease population. in addition, the brains of patients with Alzheimer disease than non-Alzheimer's patients contain less IL-33."
"Despite the excitement, there is a certain distance between laboratory studies and clinical applications. In the medical field, there are enough false 'breakthrough' warning us that before the completion of rigorous clinical trials, we should hold our breath. We just enter the phase I clinical trials in tests of toxicity produced by a dose of IL-33. However, this is a good start."
Read more: http://www.cusabio.com/ELISA-Kit/Rabbit-arachidonic-AcidAA-ELISA-kit-1035377.html
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