Wednesday May 23, 2018

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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Cholesterol Can Increase Risk of Alzheimer’s Disease, Finds Research

In the case of Alzheimer's disease, the amyloid-beta molecules stick to the lipid cell membranes that contain cholesterol.

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

Cholesterol — a molecule normally linked with cardiovascular diseases — may also play an important role in the onset and progression of Alzheimer’s disease, researchers have found.

The findings, published in the journal Nature Chemistry, suggests that in the brain, cholesterol acts as a catalyst which triggers the formation of the toxic clusters of the amyloid-beta protein, which is a central player in the development of Alzheimer’s disease.

The researchers found that cholesterol, which is one of the main components of cell walls in neurons, can trigger amyloid-beta molecules to aggregate, and their aggregation eventually leads to the formation of amyloid plaques, in a toxic chain reaction that leads to the death of brain cells.

“The levels of amyloid-beta normally found in the brain are about a thousand times lower than we require to observe it aggregating in the laboratory – so what happens in the brain to make it aggregate?” said lead author Michele Vendruscolo, Professor at Centre for Misfolding Diseases, in the University of Cambridge.

Cholesterol -- a molecule normally linked with cardiovascular diseases -- may also play an important role in the onset and progression of Alzheimer's disease, researchers have found.
Junk Food is highly rich in Cholesterol, pixabay

For the study, using a kinetic approach, the researchers found in vitro studies that the presence of cholesterol in cell membranes can act as a trigger for the aggregation of amyloid-beta.

Since amyloid-beta is normally present in such small quantities in the brain, the molecules don’t normally find each other and stick together. Amyloid-beta does attach itself to lipid molecules, however, which are sticky and insoluble, the researcher said.

In the case of Alzheimer’s disease, the amyloid-beta molecules stick to the lipid cell membranes that contain cholesterol.

Also Read: Small Head Blows Can Also Increase Risk of Dementia 

Once stuck close together on these cell membranes, the amyloid-beta molecules have a greater chance to come into contact with each other and start to aggregate – in fact, the researchers found that cholesterol speeds up the aggregation of amyloid-beta by a factor of 20.

“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.

“We’re not saying that cholesterol is the only trigger for the aggregation process, but it’s certainly one of them,” Vendruscolo added. (IANS)

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