Wednesday December 13, 2017

Alzheimer’s experimental drug shows new hope in treatment

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New York: An experimental drug has been found to protect Alzheimer’s-inflicted mice from memory deterioration, despite a high-glycemic-index (GI) diet meant to boost blood sugar levels.

The experimental drug from the US-based Eli Lilly and Company mimics the hunger-signalling hormone ghrelin.

“The present results suggest that ghrelin might improve cognition in Alzheimer’s disease via a central nervous system mechanism involving insulin signalling,” authors of the study published in the journal Scientific Reports wrote.

“With chronic diseases like diabetes and Alzheimer’s, you need to do a long-term study,” said examiner Inga Kadish, assistant professor at University of Alabama School of Medicine at Birmingham.

“So we did an experiment with the worst-case scenario, a high GI diet. Alzheimer’s disease has 10 or 20 risk factors and some of the strongest risk factors are diabetes or metabolic syndrome.”

In contrast to short-term administration of the ghrelin agonista drug – which impairs insulin sensitivity and glucose tolerance, which are signs of metabolic syndrome and diabetes – the researchers found that the long-term ghrelin agonist treatment did not impair insulin signalling and glucose tolerance in Alzheimer’s disease mice fed with a high GI diet.

In the study, the Alzheimer’s disease-model mice showed a deterioration in spatial learning as they turned older — in other words, they got lost when trying to swim to a platform hidden just beneath the water surface that they previously were trained to find in a four-foot-wide pool.

The test mice fed with the ghrelin agonist and the high-GI diet showed long-term cognitive enhancement in this water maze test as compared to the mice fed with a normal diet or high-GI diet only.

The test mice also showed more activity, reduced body weight and fat mass. They also showed a beneficial impact of the long-term ghrelin agonist treatment on insulin signalling pathways in hippocampal brain tissue.

Alzheimer’s patients show significant shrinkage of the hippocampus, a part of the brain cortex that has a key role in forming new memories. (IANS)

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This drink may help ward off Alzheimer’s: Scientist

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Alzheimer's disease. Wikipedia

New York, October 31’2017: Researchers from the Massachusetts Institute of Technology (MIT) have developed a nutrient mix that has shown potential to slow down cognitive impairment in the early stages of Alzheimer’s disease.

The drink, called Souvenaid is aimed at treating “the root cause” of Alzheimer’s, which is the loss of brain synapses.

 Souvenaid contains omega-3 fatty acids found in oily fish like salmon and mackeral along with high doses of Vitamin B13, B, C and E.

The mixture increases production of new synapses and restores connectivity between brain regions, improving memory and other cognitive functions, the researchers reported, in the MIT Technology Review.

In the new clinical trial, published in the journal Lancet Neurology, the team conducted a 24-month trial, where more than 300 patients with prodromal Alzheimer’s — the predementia stage of Alzheimer’s with mild symptoms — were randomly assigned Souvenaid or a placebo.

The patients taking Souvenaid showed about 45 per cent less cognitive decline than people taking the placebo.

Patients who drank Souvenaid showed less worsening in everyday cognitive and functional performance and improvement in verbal-memory performance.

“It feels like science-fiction, where you can take a drink of Souvenaid and you get more synapses…for improved cognitive function. But it works,” said Richard Wurtman, Professor at the Massachusetts Institute of Technology in Boston.

Importantly, Souvenaid led to a 26 per cent reduction in the loss of hippocampal volume, which is caused early in Alzheimer’s by brain tissue loss.

The results indicate that Souvenaid may be able to slow or stop full progression of very early Alzheimer’s into a full-blown disease, Wurtman noted.

The findings could encourage more researchers to view synapse restoration as a treatment for Alzheimer’s.

“Everyone who writes about Alzheimer’s knows there’s a synapse deficiency, and this impairs connections between brain regions. Even if the amyloid or another problem gets solved, one way or another, you’ll have to replace these synapses,” Wurtman said.(IANS)

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Multi-gene Test Found Effective in Predicting Alzheimer’s Dementia

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Alzheimer Disease. IANS

San Francisco, Sep 24, 2017:  In a new test, a research team has found that combining the effects of over two dozen genetic variants help in predicting which cognitively normal older adults will go on to develop Alzheimer’s dementia.

The advantage of the test, known as Polygenic Hazard Score (PHS), is relative to testing only for the well-known genetic variant APOE E4, which has been considered the strongest genetic predictor of whether someone is likely to develop Alzheimer’s — a chronic neurodegenerative disease that usually starts slowly and worsens over time.

However, APOE E4 is only carried by 10 to 15 per cent of the population and recent research suggests that its effects have been overstated, Xinhua news agency reported on Sunday.

Publishing their findings this week in Annals of Neurology, the team, led by researchers at the University of California, San Francisco (UCSF), and the University of California, San Diego, believes that the PHS test could provide risk estimates for the remaining 85 to 90 per cent of people who do not carry at least one copy of APOE E4.

Also Read: Yoga and these 5 Foods Prevent from Alzheimer’s & Will Boost your Memory 

“Beyond APOE E4 by itself, our polygenic hazard score can identify cognitively normal and mildly impaired older folks who are at greatest risk for developing Alzheimer’s associated clinical decline over time,” Chin Hong Tan from UCSF and the paper’s first author was quoted as saying.

Researchers found that PHS test could predict how long it would take for them to progress to Alzheimer’s dementia and how steep their cognitive decline would be.

The test enables the researchers to calculate an age-specific risk of developing Alzheimer’s based upon each person’s share of 31 genetic variants plus APOE E4. (IANS)

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Air pollution can Increase Risk of Dementia in Elder Women: Study

These women were also 92 per cent more likely to develop dementia, including Alzheimer's.

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New York, Feb 1, 2017: Elderly women exposed to tiny air pollution particles may face an increased risk of dementia, including Alzheimer’s disease, a study has found.

The findings showed the fine particulate matter (PM 2.5) — coming from power and automobile plants — could invade the brain and wreak havoc in older women who live in these places.

The air quality of those places which exceeds the US Environmental Protection Agency’s standard of 81 percent were more likely to experience global cognitive decline.

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These women were also 92 per cent more likely to develop dementia, including Alzheimer’s.

“Microscopic particles generated by fossil fuels get into our body directly through the nose into the brain,” said Caleb Finch, Professor at the University of Southern California (USC).

“Cells in the brain treat these particles as invaders and react with inflammatory responses, which over the course of time, appear to exacerbate and promote Alzheimer’s disease,” Finch added.

The effects were stronger in women who had the APOE4 gene — a genetic variation that increases the risk for Alzheimer’s.

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For the general population, the risk was nearly 21 per cent, the researchers said.

The study also “provides the evidence of a critical Alzheimer’s risk gene possibly interacting with air particles to accelerate brain ageing,” said Jiu-Chiuan Chen, Associate Professor at the USC.

For the study, published in the Nature journal Translational Psychiatry, the team analysed data of 3,647 of 65- to 79-year-old women who did not have dementia.

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In another experiment, the scientists chronically exposed female mice carrying the APOE4 gene to nano-sized air pollution for 15 weeks.

The results showed that the exposure of mice to air particles damaged neurons in the hippocampus — the memory centre vulnerable to both brain ageing and Alzheimer’s disease.

-IANS