Health Discovery of new active compounds against Alzheimer''s disease

Here is a great dementia resource for caregivers and healthcare professionals,

You will love the Amazon Kindle Fire

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Follow Alzheimers1 on twitter

ENEVA,(KUNA) -- Based on computer simulations, biochemists from the University of Zurich in Switzerland have shown on Tuesday shown how the active compounds and fragments of the peptide, that causes Alzheimer disease, interact with each other and found that it is the disordered structure of the peptide that determines the interactions with active compounds.
"Various molecules have been synthesized that inhibit self-assembly of the amyloid beta peptide in vitro. This peptide is strongly linked to Alzheimer's disease," said Dr. Andreas Vitalis to KUNA.
Dr. Vitalis said that more than half of all cases of dementia in the elderly can be attributed to Alzheimer's disease, adding that despite vast research efforts; an effective therapy has not been developed, and treatment consists of dealing with the symptoms.
He noted that changes in brain tissues are a hallmark of Alzheimer's. In affected individuals, small protein fragments known as amyloid beta peptides accumulate and are deposited in the gray brain matter, said Dr.Vitalis.
Researchers recently identified a series of synthetic compounds (inhibitors) that interfere with the self-assembly of the amyloid beta peptide in vitro; they influence both early stages and the transition to the characteristic amyloid fibrils.
On a theoretical level, these compounds thus satisfy an initial condition for the development of an Alzheimer drug.
In order to understand the interactions between the amyloid beta peptide and active compounds at a structural level, Marino Convertino, Andreas Vitalis, and Amedeo Caflisch from the University of Zurich's Department of Biochemistry simulated these interactions on the computer.
"In doing so, we focused on a fragment of the peptide that is thought to control both interactions with inhibitors and progression of disease," Dr.
Vitalis explained to KUNA.
Based on these simulations, the biochemists were able to identify a hierarchy of interaction patterns between the peptide and various active compounds. To their surprise, they discovered that the disordered structure of the peptide controls the interactions.
"The peptide's disorder and flexibility enable it to adapt to many basic structural frameworks," Dr.Vitalis explained.
Often it is only subparts of the molecules that mediate interactions on the compound side. However, even minimal changes to a compound may induce measurable changes to the peptide-compound interactions.
"Design of active compounds that influence the amyloid beta peptide structurally in a specific manner will only be possible with the aid of high-resolution methods that are limited to one or a few molecules," concludes Vitalis.
In the next step, the researchers from the University of Zurich want to identify new classes of active substances with controllable properties that interact with the amyloid beta peptide

Is Alzheimer's Disease Contageous?

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here is a way for nurses administrators, social workers and other health care professionals to get an easyceu or two

Here are more interesting dementia brain boosting activities





Get your subscription to Activity Director Today's e magazine" />

Digital Journal

Alzheimer's disease is caused partly by the build-up of abnormal proteins in the brain. Scientists already know that one of these abnormal proteins, amyloid peptides also called beta amyloids, can be infectious.
It seems that Alzheimer’s disease is easier to catch than first thought.

Neurologist Yvonne S. Eisele and her team of fellow scientists had already proved that mice could catch Alzheimer’s disease from each other; however this only happened when the brain of a healthy mouse was injected with amyloid peptides from mice that already had Alzheimer's disease symptoms.
Now a new study shows about Is Alzheimer's Diseaase Contageous

Alzheimer's chemicals may be natural part of brain function

Here is a great dementia resource for caregivers and healthcare professinals,

Here is information on being the best caregiver you can be

Here are more interesting dementia brain boosting activities

Deseret News

By Elizabeth Stuart

natural part of human brain function, recent research suggests.

"You are actively forgetting and remembering all the time," said Dr. Dale Bredesen, founding president and CEO of the Buck Institute for Age Research, during a presentation Tuesday at the University of Utah. "Alzheimer's disease is just a fundamental imbalance in those signals."

Most researchers look at Alzheimer's as a disease of toxicity, said Bredesen, who works out of Novato, Calif.

"It's like having acid on your brain," he said. "Something's eating it."

But the chemical associated with tissue destruction in Alzheimer's patients is also present in the brains of young, healthy people — a phenomenon none of the more than 500,000 scientific papers published on the topic can explain.

"We argue the amyloid beta peptide does have a normal function," Bredesen said. "We think Alzheimer's is more of a signaling disorder rather than a disease of toxicity."

Bredesen's theory links brain development to brain deterioration.

As a fetus grows, it produces more nerve cells than it will ultimately use. Some of those cells build connections with one another, some die. Both outcomes are determined by naturally occurring chemicals.

Alzheimer's disease, said Bredesen, is an out-of-control example of this same process.

"The amyloid beta peptide in your brain is doing what it's supposed to do, but there's a thousand times too much of it," he said.

Bredesen and his colleagues believe netrin-1, another naturally occurring protein, has the opposite effect as amyloid beta peptide.

Preliminary lab tests using mice infected with "Mouzheimer's" support this theory. After just 10 days of treatment, mice injected with netrin-1 showed behavioral improvement.

"The idea is if you insert amyloid beta peptide into the receptor, it'll tell your nerve cell to start packing up and moving out," he said. "When you insert netrin-1, the cell gets the signal to start setting up for a party