Monday February 19, 2018

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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A study finds: What causes dementia?

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1 in 6 people over the age of 80 have dementia. Pixabay
1 in 6 people over the age of 80 have dementia. Pixabay

Dementia results in a progressive and irreversible loss of nerve cells and brain functioning, causing loss of memory and cognitive impairments affecting the ability to learn. Currently, there is no cure.

Findings

  • The toxic build-up of urea, a compound created by the liver, in the brain has been found as the major reason that can cause brain damage and lead to Huntington’s Disease, one of seven major types of age-related dementia.
  • Urea level peaks in the brain even before dementia sets in. The discovery could one day help doctors diagnose and even treat dementia.
  • Urea is similarly linked to Alzheimer’s, suggesting that the toxic build-up of urea could be relevant to all types of age-related dementias.
44 million people worldwide suffer from dementia. Pixabay
44 million people worldwide suffer from dementia. Pixabay

“This study on Huntington’s Disease is the final piece of the jigsaw which leads us to conclude that high brain urea plays a pivotal role in dementia,” said Garth Cooper, Professor at The University of Manchester.

“Alzheimer’s and Huntington’s are at opposite ends of the dementia spectrum — so if this holds true for these types, then I believe it is highly likely it will hold true for all the major age-related dementias,” Cooper said, in the paper published in the Proceedings of the National Academy of Sciences.

Urea and ammonia in the brain are metabolic breakdown products of protein. If urea and ammonia build up in the body because the kidneys are unable to eliminate them, for example, serious symptoms can result, the researchers said.

“More research, however, is needed to discover the source of the elevated urea in Huntington’s Disease, particularly concerning the potential involvement of ammonia and a systemic metabolic defect,” Cooper noted.

For the study, the team used human brains, donated by families for medical research, as well as transgenic sheep in Australia.

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