Friday March 22, 2019

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)

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Eye Test May Help in Early Detection of Alzheimer’s Disease

Conversely, in the eyes of 39 people with Alzheimer's disease, that web was less dense and even sparse in places

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

A future non-invasive eye test may allow early detection of Alzheimer’s disease before memory loss kicks in, say a team led by an Indian-origin researcher.

Retina being an extension of the brain, the optical coherence tomography angiography (OCTA) will check patients’ vision as well as brain health, said the study published in the journal Ophthalmology Retina.

The researchers said that loss of blood vessels in retina would reflect changes in the brain, be it for both healthy people or Alzheimer’s patients.

“We know that there are changes that occur in the brain in the small blood vessels in people with Alzheimer’s disease, and because the retina is an extension of the brain, we wanted to investigate whether these changes could be detected,” said lead author Dilraj S. Grewal, ophthalmologist at Duke University.

Using the OCTA that uses light waves that reveal blood flow in every layer of the retina, the researches checked more than 200 people.

A lady suffering from Alzheimer’s. Flickr

They found that in people with healthy brains, microscopic blood vessels form a dense web at the back of the eye inside the retina — as was seen in 133 participants in a control group.

Conversely, in the eyes of 39 people with Alzheimer’s disease, that web was less dense and even sparse in places.

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The OCTA machines, relatively a new noninvasive technology, measures blood vessels that cannot be seen during a regular eye examination.

“It’s possible that these changes in blood vessel density in the retina could mirror what’s going on in the tiny blood vessels in the brain, perhaps before we are able to detect any changes in cognition,” added Sharon Fekrat, ophthalmologist at the Duke University in the US. (IANS)