A new medication for Alzheimers?

CBS local in New York reports,

Although their goal was to cure diabetes, scientists may have stumbled onto a new medication to help treat the devastating effects of Alzheimer’s disease.

According to a press release from researchers at Lancaster University, a new drug being tested for diabetes patients was found to have “significantly reversed memory loss” in test subjects and is now being examined as possible treatment for neurodegenerative disorders.

The medication, known as a triple receptor drug — or “triple agonist” — reportedly works in multiple ways to protect the brain against degeneration and promote growth. Researchers say that a study of mice being given the drug found that the animals had an increased ability to learn and retain memories.

“These very promising outcomes demonstrate the efficacy of these novel multiple receptor drugs that originally were developed to treat type 2 diabetes,” Professor Christian Holscher said in the release.

The scientists added that the mice showed a decrease in chronic inflammation and amyloid plaques in the brain, which have been linked to the development of Alzheimer’s in people.

“With no new treatments in nearly 15 years, we need to find new ways of tackling Alzheimer’s,” Dr. Doug Brown of the Alzheimer’s Society said. “It’s imperative that we explore whether drugs developed to treat other conditions can benefit people with Alzheimer’s.”

The discovery of the diabetes drug’s side-effect is not a complete coincidence to the researchers. The findings, published in the journal Brain Research, point to the link between some of the symptoms of diabetes and their link to Alzheimer’s. Insulin desensitisation is not only one of the key effects suffered by diabetes patients, the hormone’s lack of production has also reportedly been observed in the brains of people affected by the memory-stealing disorder.

"Researchers discovered a specific protein — SIRT6 — is severely reduced in the brains of Alzheimer’s patients."

At the website entitled American Associates Ben-Gurion University of the Negev, we learn

Alzheimer’s disease, the most common cause of dementia, afflicts 10 percent of those over the age of 65. Now, researchers at Ben-Gurion University have learned what may trigger it.

The researchers discovered a specific protein — SIRT6 — is severely reduced in the brains of Alzheimer’s patients. SIRT6 is critical to the repair of DNA, the deterioration of which “is the beginning of the chain that ends in neurodegenerative diseases in seniors,” explains Dr. Debbie Toiber, lead author on the study and a member of the BGU Department of Life Sciences.

“We should be focusing our research on how to maintain production of SIRT6 and improve the repair capacity of the DNA damage that leads to these diseases,“ Dr. Toiber says.

Dr. Toiber’s lab research is focused on DNA damage as the cause of aging and age-related diseases. She and her team discovered that as a person ages the amount of the SIRT6 protein in the brain declines.

“In Alzheimer’s patients, it is almost completely gone,” she says.

Unfortunately, it is not enough to simply inject the protein into the brain to replenish its supply.

“There is a blood brain barrier that prevents things from passing into it,” Dr. Toiber explains. “But we are trying to find a way to increase the expression of the protein into the brain.”

DNA in each cell breaks down due to natural causes, such as metabolism and the usage of the DNA to produce proteins.

According to Dr. Toiber, we damage DNA just through normal living. “We repair it and continue going on. But the repairs are not perfect and some DNA remains unrepaired. As you get older unrepaired DNA accumulates.”

When the DNA is damaged, Dr. Toiber explains, it may lose important information. “If a cell feels it is too dangerous to continue with this damaged DNA, it may activate a self-destruct mechanism. If too many cells do this, the tissue with the dying cells will deteriorate, such as the brain.”

Dr. Toiber acknowledges that healthy habits like good diet and exercise might make a difference in our DNA health, but there is little we can do to avoid the effects of aging entirely.

“You have to remember that half of everyone over the age of 95 will get Alzheimer’s,” she says. “It is not something genetic or environmental. That may influence it a little bit, but when there is a 50-50 chance of getting Alzheimer’s, it demonstrates that it just happens over a lifetime.”

Still, Toiber is quick to point out that engaging in sports and even working past retirement can challenge the body in positive ways, preparing your cells to react more readily and thus be more likely able to repair themselves.

Hope for Alzheimer's, Parkinson's and Schizophrenia sufferers

In a mouse model of Alzheimer's disease, Salk Institute researchers show that raising levels of neuregulin-1 (right) lowers a marker of disease pathology in a part of the brain that controls memory compared with controls (left). Credit: Salk Institute

Medical Express reports

Boosting levels of a specific protein in the brain alleviates hallmark features of Alzheimer's disease in a mouse model of the disorder, according to new research published online August 25, 2016 in Scientific Reports.
The protein, called neuregulin-1, has many forms and functions across the brain and is already a potential target for brain disorders such as Parkinson's disease, amyotrophic lateral sclerosis and schizophrenia.

Read more here.

An open letter to Will Ferrell

Patti Davis, daughter of Ronald Reagan, has written an open letter here to Will Farrell, who plans to make a comedy about President Reagan in the throes of Alzheimers.

Faster, please!

Sarah Knapton writes:

Alzheimer's could be prevented and even cured by boosting the brain's own immune response, scientists at Stanford University believe.

Researchers discovered that nerve cells die because cells which are supposed to clear the brain of bacteria, viruses and dangerous deposits, stop working.

These cells, called 'microglia' function well when people are young, but when they age, a single protein called EP2 stops them operating efficiently.

Now scientists have shown that blocking the protein allows the microglia to function normally again so they can hoover up the dangerous sticky amyloid-beta plaques which damage nerve cells in Alzheimer's disease.

The researchers found that, in mice, blocking EP2 with a drug reversed memory loss and myriad other Alzheimer’s-like features in the animals.

The scientists discovered that in young mice, the microglia kept the sticky plaques under control. But when experiments were done on older mice, the protein EP2 swung into action and stopped the microglia producing enzymes which digested the plaques.

Similarly mice which were genetically engineered not to have EP2 did not develop Alzheimer's disease, even when injected with a solution of amyloid-beta, suggesting that their cells were getting rid of the protein naturally.

And for those mice who developed Alzheimer's, blocking EP2 reversed memory decline.

Now Stanford is hoping to produce a compound which only blocks EP2 to prevent unnecessary side effects.

Read more here.

Thanks to Carl Huffman

Alzheimers Disease now affects one in nine Americans over age 65

When does Alzheimers Disease show up?


Electra Draper writes:

As many as 5.2 million Americans age 65 and older have the incurable dementia-causing disease — a number that could triple by 2050 because of population trends. About half of those age 85 and older have Alzheimer's.

Last month, Denver Broncos owner Pat Bowlen, 70, relinquished control of the football team as his family and the organization announced that he has the disease.

Most people with Alzheimer's live four to eight years after diagnosis, but many survive 20 years.

Read more here.