Friday September 21, 2018

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
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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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Scientists Discover A New Method To Fight Alzheimer’s, Dementia

Worldwide, about seven percent of people over 65 suffer from Alzheimer's or some form of dementia, a percentage that rises to 40 percent above the age of 85.

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Alzheimer's
One hemisphere of a healthy brain (L) is pictured next to one hemisphere of a brain of a person suffering from Alzheimer disease. VOA
Eliminating dead-but-toxic cells occurring naturally in the brains of mice designed to mimic Alzheimer’s slowed neuron damage and memory loss associated with the disease, according to a study published Wednesday that could open a new front in the fight against dementia.The accumulation in the body of “zombie cells” that can no longer divide but still cause harm to other healthy cells, a process called senescence, is common to all mammals.

Scientists have long known that these dead-beat cells gather in regions of the brain linked to old age diseases ranging from osteoarthritis and atherosclerosis to Parkinson’s and dementia.

Prior research had also shown that the elimination of senescent cells in ageing mice extended their healthy lifespan.

But the new results, published in Nature, are the first to demonstrate a cause-and-effect link with a specific disease, Alzheimer’s, the scientists said.

Alzheimer's
A lady suffering from Alzheimer’s. Flickr

But any treatments that might emerge from the research are many years down the road, they cautioned.

In experiments, a team led by Tyler Bussian of the Mayo Clinic in Rochester, Minnesota used mice genetically modified to produce the destructive, cobweb-like tangles of tau protein that form in the neurons of Alzheimer’s patients.

The mice were also programmed to allow for the elimination of “zombie” cells in the same region.

“When senescent cells were removed, we found that the diseased animals retained the ability to form memories, and eliminated signs of inflammation,” said senior author Darren Baker, also from the Mayo Clinic.

The mice likewise failed to develop Alzheimer’s signature protein “tangles”, and retained normal brain mass.

 

Alzheimer's
Alzheimer’s disease patient Isidora Tomaz, 82, sits in an armchair in her house in Lisbon, Portugal. It’s predicted that by 2050, 135 million Americans are going to suffer from mild cognitive impairment, a precursor of Alzheimer’s. VOA

Keeping zombies at bay

A closer look revealed that the “zombies” belonged to a class of cells in the brain and spinal cord, called glia, that provide crucial support and insulation to neurons.

“Preventing the build-up of senescent glia can block the cognitive decline and neuro-degeneration normally experienced by these mice,” Jay Penney and Li-Huei Tsai, both from MIT, wrote in a comment, also in Nature.

Bussian and his team duplicated the results with pharmaceuticals, suggesting that drugs could one day slow or block the emergence of Alzheimer’s by keeping these zombie cells at bay.

“There hasn’t been a new dementia drug in 15 years, so it’s exciting to see the results of this promising study in mice,” said James Pickett, head of research at Alzheimer’s Society in London.

 

Alzheimer's
The accumulation in the body of “zombie cells” that can no longer divide but still cause harm to other healthy cells, a process called senescence, is common to all mammals. IANS

For Lawrence Rajendran, deputy director of the Dementia Research Institute at King’s College London, the findings “open up new vistas for both diagnosis and therapy for neurodegenerative diseases, including Alzheimer’s.”

Up to now, dementia research has been mostly focused on the diseased neurons rather than their neighboring cells.

“It is increasingly becoming clear that other brains cells play a defining role,” Rajendran added.

Several barriers remain before the breakthrough can be translated into a “safe, effective treatment in people,” Pickett and other said.

The elderly often have lots of harmless brain cells that look like the dangerous senescent cells a drug would target, so the molecule would have to be good at telling the two apart.

Also Read: Common Painkillers Triple Harmful Side Effects in Dementia

Worldwide, about seven percent of people over 65 suffer from Alzheimer’s or some form of dementia, a percentage that rises to 40 percent above the age of 85.

The number afflicted is expected to triple by 2050 to 152 million, according to the World Health Organization, posing a huge challenge to healthcare systems. (VOA)