Our opinion: A reason to look forward to 2015

Posted

While it might be easy to conclude 2015 has gotten off to a rocky start, this might turn out to be an extraordinary year for more than 40 million people and their families.

Late last year, researchers at Stanford University announced the results of a study that could prove to be a turning point in the world's battle against the wasting away that is visited upon those suffering from Alzheimer's Disease. Their research concluded Alzheimer's could be prevent or even cured by boosting the brain's immune response.

According to the researchers, as we age, nerve cells in our brains die because "microglia" cells, which clear the brain of bacteria, viruses and dangerous deposits, stop working.

"Microglia are the brain's beat cops," said Dr Katrin Andreasson, professor of neurology and neurological sciences at Stanford University School of Medicine. "Our experiments show that keeping them on the right track counters memory loss and preserves healthy brain physiology."

But microglia are prevented from doing its job by the EP2 protein. The researchers discovered if they can block the protein, microglia can return to its job of cleaning up sticky amyloid-beta plaques which damage nerve cells in Alzheimer's disease.

According to Alzheimer's Disease International, 7.7 million new cases of dementia are diagnosed each year. If the epidemic is not contained, but 2050 it is expected to afflict more than 135 million people. Currently, Alzheimer's worldwide cost is more than $600 billion a year (or about 1 percent of the world's gross domestic product), which includes informal care (unpaid care provided by family and others), direct costs of social care (provided by community care professionals, and in residential home settings) and the direct costs of medical care (the costs of treating dementia and other conditions in primary and secondary care).

Microglia constitute about 10 to 15 percent of all the cells in the brain, and are "the brain's beat cops," said Andreasson. "The microglia are supposed to be, from the get-go, constantly clearing amyloid-beta, as well as keeping a lid on inflammation. If they lose their ability to function, things get out of control. A-beta builds up in the brain, inducing toxic inflammation."

According to the Stanford University School of Medicine, microglia also protect the brain against invading bacteria and viruses by gobbling them up.

"They are adept at calming things down, too, clamping down on inflammation if it gets out of hand. They also work as garbage collectors, chewing up dead cells and molecular debris strewn among living cells — including clusters of a protein called A-beta, notorious for aggregating into gummy deposits called Alzheimer's plaques, the disease's hallmark anatomical feature."

When A-beta clumps into soluble clusters consisting of a few molecules, it's highly toxic to nerve cells, and are believed to play a substantial role in causing Alzheimer's.

"The microglia are supposed to be, from the get-go, constantly clearing A-beta, as well as keeping a lid on inflammation," Andreasson said.

A receptor protein called EP2 has a strong potential to cause inflammation when activated by binding to a substance called prostaglandin E2, or PGE2. The experiments first started in a petri dish and then expanded into mice. When EP2 was blocked, microglia were able to resume their duties. The mice responded well to the treatment, according to the report.

The next step will be to determine if an EP2 blocker is safe for human trials. As with any new or alternative therapy, people will line up for treatment, but due to the complexities of Alzheimer's researchers will have to be cautious about who qualifies. Nonetheless, this is very good news for the millions of people suffering from this debilitating illness. It's also very good news for the families who are struggling to care for loved ones who have slipped or are slipping away as the disease progresses.


TALK TO US

If you'd like to leave a comment (or a tip or a question) about this story with the editors, please email us. We also welcome letters to the editor for publication; you can do that by filling out our letters form and submitting it to the newsroom.



Powered by Creative Circle Media Solutions