Diabetes news Potential cures Type 3 (Alzheimer's)

New hope in the war on dementia as scientists discover diabetes drug may also reverse memory loss

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Scientists at Lancaster University found the treatment – called a triple receptor agonist – significantly improved memory and reduced toxins in the brain when tested on mice / Photo via Daily Mail

A daily injection of a drug initially developed for diabetes may reverse Alzheimer’s, early research suggests.

Scientists at Lancaster University found the treatment – called a triple receptor agonist – significantly improved memory and reduced toxins in the brain when tested on mice.

Experts last night said the drug has ‘clear promise’ to eventually become the first treatment to tackle Alzheimer’s.

The drug is some way off becoming available to patients, having only been tested on animals so far, but if it shows the same results in humans it could in time solve the desperate need for an effective treatment for the booming number of people suffering from Alzheimer’s. Dr Doug Brown, director of research at the Alzheimer’s Society which funded the study, 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. Further development of this work is crucial.’

The treatment contains three hormones which work in a triple attack against different causes of Alzheimer’s.

The three hormones are already separately used to treat type two diabetes, because they improve the body’s sensitivity to insulin.

But researchers found in recent trials they are more effective as a combination therapy. The study, however, shows the triple jab could play a far more significant role as a dementia treatment. The results, published in the Brain Research journal, found it improved learning and memory formation in mice with Alzheimer’s.

It also resulted in reduced levels of amyloid, a sticky protein which forms plaques in the brain, and reduced chronic inflammation and oxidative stress. The scientists found the drug also slowed down the rate of nerve cell loss, a key marker of dementia.

Lead researcher Professor Christian Holscher said:

‘[This] holds clear promise of being developed into a new treatment for chronic neurodegenerative disorders such as Alzheimer’s disease.

‘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.’

Scientists are particularly excited about the development because of a string of failures of major drugs which they had hoped would provide a breakthrough in dementia treatment.

The failed drugs each focused solely on tackling amyloid.

But the triple receptor agonist – which contains the hormones GLP-1, GIP and Glucagon – seems to cover more bases by also boosting insulin, which is known to protect the brain, and also reduce inflammation, oxidative damage and nerve dieback.

Last year the Office for National Statistics announced dementia had become the biggest cause of death in England and Wales.

An estimated 850,000 in the UK are thought to be living with dementia, with figures expected to rise to one million by 2025.

Dr David Reynolds, chief scientific officer at Alzheimer’s Research UK, said:

‘Future studies will need to build on these findings to further assess the potential of this drug and its suitability for testing in people.’

Alzheimer's treatment
Fig. 1. The novel TA improved the learning ability of APP/PS1 mice in the spatial water maze task. (A) The escape latency and swimming speed in the training trails. (B) The percentage of time in target quadrant and crossing platform times in the probe trials. The circle indicates the position of the platform during acquisition (C) Representative swimming tracks of the probe trial. * = P < .05, ** = P < .01 compared to the control group, ## = P < .01, # = P < .05 compared to the APP/PS1 group; Two-way ANOVA with Bonferroni repeated measures post hoc tests.
Alzheimer's treatment
Fig. 2. TA treatment reduced amyloid deposits in the cortex and hippocampus of APP/PS1 mice. A, D: control group; B, E: APP/PS1 group; C, F: APP/PS1+TA group. Scale bar in image D: 100 μm. *** = P < .001 compared to the control group; ### = P < .001 compared to the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures post hoc tests. N = 6 per group. / Photo via Brain Research
Fig. 3. TA-treatment reduced the number of GFAP positive cells in the cortex and hippocampus of APP/PS1 mice. A, D: control group; B, E: APP/PS1 group; C, F: APP/PS1+TA. Scale bar in image D: 50μm. A higher magnification image has been added to show stained astroglia. *** = P < .001 compared with the control group; ### = P < .001 compared with the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures post hoc tests. N = 6 per group. / Photo via Brain Research
Alzheimer's treatment
Fig. 4. TA treatment reversed the increase of IBA-1 positive cells in the cortex and hippocampus of APP/PS1 mice. A, D: control group; B, E: APP/PS1 group; C, F: APP/PS1+TA group. Scale bar in image D: 100 μm. A higher magnification image has been added to show stained microglia. *** = P < .001 compared to the control group; ## = P < .01, ### = P < .001 compared to the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures post hoc tests. N = 6 per group. / Photo via Brain Research
Alzheimer's treatment
Fig. 5. Oxidative stress was reduced by the TA. 5A. TA-treatment reduced the increase of 4-HNE levels in the cortex and hippocampus in APP/PS1 mice. A, D: control group; B, E: APP/PS1 group; C, F: APP/PS1+TA group. Scale bar in image D: 100 μm. *** = P < .001 compared with controls; ###=P < .001 compared to the APP/PS1 group. 5B. TA treatment reduced the increase of 8-OHdG levels in the cortex and hippocampus of APP/PS1 mice. A, D: control group; B, E: APP/PS1 group; C, F: APP/PS1+TA group. Scale bar in image D: 100 μm. *** = P < .001 compared to the control group; ## = P < .01, ### = P < .001 compared with the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures ***post hoc tests. N = 6 per group. / Photo via Brain Research
Alzheimer's treatment
Fig. 6. TA-treatment enhanced neurogenesis and increased numbers of DCX positive cell numbers in the dentate gyrus of APP/PS1 mice. A: control group; B: APP/PS1 group; C: APP/PS1+TA group. Scale bar in image A: 100 μm. *** = P < .001 compared with the control group; ### = P < .001 compared with the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures post hoc tests. N = 6 per group. / Photo via Brain Research
Alzheimer's treatment
Fig. 7. A) TA-treatment increased levels of BDNF in the hippocampus of APP/PS1 mice. *** = P < .001compared with the control group; # = P < .05 compared with the APP/PS1 group. N = 6 per group. B) TA-treatment increased levels of synaptophysin in the hippocampus of APP/PS1 mice. *** = P < .001 compared with the control group; ## = P < .01 compared with the APP/PS1 group. N = 6 per group. C) TA-treatment increased the ratio of BAX/Bcl-2 in the hippocampus of APP/PS1 mice. *** = P < .001 compared with the control group; ### = P < .001 compared with the APP/PS1 group. One-way ANOVA with Bonferroni repeated measures post hoc tests. N = 6 per group. / Photo via Brain Research

Originally published at Brain Research, edited by Ben Spencer for Daily Mail


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