Wednesday February 20, 2019

Managing Cholesterol Might Help To Reduce Alzheimer’s Risk

These included several points within the CELF1/MTCH2/SPI1 region on chromosome 11 that previously had been linked to the immune system

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Poor sleep can predict Alzheimer's Risk in elderly. Pixabay

Managing cholesterol might help reduce Alzheimer’s risk, says researchers, including one of Indian-origin, who identified a genetic link between the progressive brain disorder and heart disease.

Examining DNA from more than 1.5 million people, the study showed that risk factors for heart disease such as elevated triglyceride and cholesterol levels (HDL, LDL, and total cholesterol) were genetically related to Alzheimer’s risk.

However, genes that contribute to other cardiovascular risk factors, like body mass index and Type-2 diabetes, did not seem to contribute to genetic risk for Alzheimer’s.

“The genes that influenced lipid metabolism were the ones that also were related to Alzheimer’s disease risk,” said Celeste M. Karch, Assistant Professor at the Washington University’s School of Medicine.

Thus, if the right genes and proteins could be targeted, it may be possible to lower the risk for Alzheimer’s disease in some people by managing their cholesterol and triglycerides, added Rahul S. Desikan, Assistant Professor at the UCSF.

For the study, published in the journal Acta Neuropathologica, the team identified points of DNA that increase the risk of cardiovascular disease and also heighten the risk for Alzheimer’s disease.

"The question for us now is not how to eliminate cholesterol from the brain, but about how to control cholesterol's role in Alzheimer's disease through the regulation of its interaction with amyloid-beta," Vendruscolo said.
In Alzheimer’s disease, patients start losing memory, Pixabay

The team looked at differences in the DNA of people with factors that contribute to heart disease or Alzheimer’s disease and identified 90 points across the genome that were associated with risk for both diseases.

Their analysis confirmed that six of the 90 regions had very strong effects on Alzheimer’s and heightened blood lipid levels, including several within genes that had not previously been linked to dementia risk.

These included several points within the CELF1/MTCH2/SPI1 region on chromosome 11 that previously had been linked to the immune system.

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The researchers confirmed their findings in a large genetic study of healthy adults by showing that these same risk factors were more common in people with a family history of Alzheimer’s, even though they had not themselves developed dementia or other symptoms such as memory loss.

“These results imply that cardiovascular and Alzheimer’s pathology co-occur because they are linked genetically. That is, if you carry this handful of gene variants, you may be at risk not only for heart disease but also for Alzheimer’s,” Desikan said. (IANS)

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Researchers Identify New Mechanism to Prevent Alzheimer’s

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K

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In Alzheimer's disease, patients start losing memory, Pixabay

Researchers have identified a novel mechanism and a potential new therapeutic target for Alzheimer’s disease (AD), says a new study on mice.

Alzheimer’s is characterised by profound memory loss and synaptic failure. Although the exact cause of the disease remains unclear, it is well established that maintaining memory and synaptic plasticity requires protein synthesis.

The function of the synapse is to transfer electric activity (information) from one cell to another.

“Alzheimer’s is such a devastating disease and currently there is no cure or effective therapy for it,” said Tao Ma, Assistant Professor at Wake Forest School of Medicine in the US.

A lady suffering from Alzheimer’s. Flickr

“All completed clinical trials of new drugs have failed, so there is clearly a need for novel therapeutic targets for potential treatments.”

For the study, the team has shown that AD-associated activation of a signaling molecule termed eEF2K leads to inhibition of protein synthesis.

Further, they wanted to determine if suppression of eEF2K could improve protein synthesis capacity, consequently alleviating the cognitive and synaptic impairments associated with the disease.

They used a genetic approach to repress the activity of eEF2K in Alzheimer’s mouse models.

Cognitive Impairment
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. VOA

The findings, published in the Journal of Clinical Investigation, showed that genetic suppression of eEF2K prevented memory loss in those animal models and significantly improved synaptic function.

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“These findings are encouraging and provide a new pathway for further research,” said Ma.

The team next plans to test this approach in additional animal studies and eventually in human trials using small molecule inhibitors targeting eEF2K. (IANS)