Wednesday February 21, 2018

This drink may help ward off Alzheimer’s: Scientist

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Alzheimer's disease. Wikipedia
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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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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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