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Monday, January 8, 2018

糖尿病 多受體藥 (GLP-1, GIP and Glucagon) 保護神經&減緩阿茲海默症!


糖尿病藥有望逆轉阿爾茨海默病患者記憶力減退 2018-01-06 09:10:56 來源: 新華網 新華社倫敦1月4日電一種用于治療II型糖尿病的藥物也許能給阿爾茨海默病患者帶來新希望。來自英國蘭開斯特大學的研究團隊日前在荷蘭《腦研究》雜志上發表報告説,這種藥物也許能改善阿爾茨海默病等慢性神經病變引發的記憶力減退。阿爾茲海默病是一種會嚴重削弱患者認知能力的漸進性腦退化病,至今仍然未有有效的治療方法。根據國際阿爾茨海默病聯合會的數據,2015年全球癡呆症患者人數估計為4680萬,這個數字到2050年可能將增至1.3億,而阿爾茨海默病佔所有癡呆症病例的一半以上。II型糖尿病可能誘發阿爾茨海默病,並影響其發病進程。胰島素受損被認為與II型糖尿病和阿爾茨海默病患者的腦萎縮過程相關。這種原用于治療II型糖尿病的藥物是一種受體激動劑藥物,它聚合了腸促胰島素GLP-1(胰高血糖素樣肽1),GIP(葡萄糖依賴性胰島素釋放肽)和升血糖激素,而這三種激素都是成長因子這也是三重受體藥物首次被用來保護大腦免于退化。之前的研究顯示,阿爾茨海默病患者大腦中的成長因子信號出現了問題。該研究採用了APP/PS1轉基因小鼠作為研究對象,它們表達誘發人類罹患阿爾茨海默病的基因。研究人員在試驗中發現,經過該藥物治療的小鼠的學習和記憶力得到了大幅改善。研究人員表示,該結果表明這種用來治療II型糖尿病的多受體藥物能有效減緩阿爾茨海默病症狀,並具有持續保護神經的效用。此前已有研究表明,有的GLP-1受體激動劑類糖尿病藥物如利拉魯肽對改善阿爾茨海默病患者的狀況確實有效,因此這種新型三重受體藥物也許能為治療阿爾茨海默病帶來新希望。

Diabetes drug 'significantly reverses memory loss' in mice with Alzheimer's

A drug developed for diabetes could be used to treat Alzheimer's; Date: January 1, 2018. A drug developed for diabetes could be used to treat Alzheimer's after scientists found it "significantly reversed memory loss" in mice through a triple method of action. The research, published in Brain Research, could bring substantial improvements in the treatment of Alzheimer's disease through the use of a drug originally created to treat type 2 diabetes. Lead researcher Professor Christian Holscher of Lancaster University in the UK said the novel treatment "holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer's disease." Alzheimer's disease is the most common cause of dementia and the numbers are expected to rise to two million people in the UK by 2051 according to Alzheimer's Society, who part- funded the research. Dr Doug Brown, Director of Research and Development at Alzheimer's Society, said: ""With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer's. It's imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer's and other forms of dementia. This approach to research could make it much quicker to get promising new drugs to the people who need them." Although the benefits of these 'triple agonist' drugs have so far only been found in mice, other studies with existing diabetes drugs such as liraglutide have shown real promise for people with Alzheimer's, so further development of this work is crucial." This is the first time that a triple receptor drug has been used which acts in multiple ways to protect the brain from degeneration. It combines GLP-1, GIP and Glucagon which are all growth factors. Problems with growth factor signalling have been shown to be impaired in the brains of Alzheimer's patients. The study used APP/PS1 mice, which are transgenic mice that express human mutated genes that cause Alzheimer's. Those genes have been found in people who have a form of Alzheimer's that can be inherited. Aged transgenic mice in the advanced stages of neurodegeneration were treated. In a maze test, learning and memory formation were much improved by the drug which also:-

ü  enhanced levels of a brain growth factor which protects nerve cell functioning

ü  reduced the amount of amyloid plaques in the brain linked with Alzheimer's

ü  reduced both chronic inflammation and oxidative stress

ü  slowed down the rate of nerve cell loss

Professor Holscher said: "These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes but have shown consistent neuro- protective effects in several studies." "Clinical studies with an older version of this drug type already showed very promising results in people with Alzheimer's disease or with mood disorders" "Here we show that a novel triple receptor drug shows promise as a potential treatment for Alzheimer's but further dose-response tests and direct comparisons with other drugs have to be conducted in order to evaluate if this new drugs is superior to previous ones." Type 2 diabetes is a risk factor for Alzheimer's and has been implicated in the progression of the disease. Impaired insulin has been linked to cerebral degenerative processes in type 2 diabetes and Alzheimer's disease. Insulin desensitisation has also been observed in the Alzheimer's disease brain. The desensitisation could play a role in the development of neurodegenerative disorders as insulin is a growth factor with neuroprotective properties.

 

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