Saturday February 16, 2019

Protective molecule against Alzheimer’s identified

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New York: Giving the search for Alzheimer’s therapies a shot in the arm, researchers have identified the steps that a molecule takes to protect the brain from toxic effects of protein fragments known as amyloid beta, a hallmark of the progressive brain disorder.

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“Our discovery centers on a protein called WAVE1, which we found to be important in the production of amyloid beta,” said study author Paul Greengard, professor at Rockefeller University in New York.

“The reduction of WAVE1 appears to have a protective effect against the disease,” Greengard noted.

Brain cells themselves make amyloid beta, and for reasons that are not fully understood, its accumulation ultimately contributes to the memory loss, personality changes, and other symptoms that patients with this degenerative disease often suffer from.

“When levels of amyloid beta rise, there is an accompanying increase in another molecule, AICD, which reduces the expression of WAVE1. This has the effect of reducing the production of amyloid beta,” Greengard explained.

“By targeting steps within this newly discovered pathway, it may be possible to develop drugs to reduce amyloid beta that potentially could be used to either treat or prevent Alzheimer’s disease,” Greengard pointed out.

WAVE1 is known to help to build filaments of a protein called actin that serve as basic components of cellular structures.

In the current study, the team, examined the levels of WAVE1 in mouse and cellular models of Alzheimer’s disease.

They found a dose-dependent response: Mice brains with low WAVE1 levels produced less amyloid-?, and these animals performed better on memory tests.

(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)