New protein helps scientists understand Alzheimer's disease

Scientists have designed a new protein to understand the reason that leads to death of nerve cells in people suffering from Alzheimer's, an advance that can help cure the disease.

In those with Alzheimer's, Amyloid-beta (Abeta) proteins stick together to make amyloid fibrils which form clumps between neurons in the brain, researchers said.

It is believed the build-up of these clumps causes brain cells to die, leading to the cognitive decline in patients suffering from the disease, they said.

It is not known why this particular protein's "stickiness" causes cells to die and scientists have been unable to properly test whether the sticky clumps of Abeta proteins have different effects, compared with individual proteins that are not stuck together.

Now, scientists from University of Sussex in the UK have created a new protein which closely resembles the Abeta protein in size and shape, but contains two different amino acids (the building blocks that proteins are made up of).

These changes mean that the new protein does not form amyloid fibres or sticky clumps, and, unlike Abeta, is not toxic to nerve cells, researchers said.

The new protein will be an essential laboratory tool for those working to understand the causes and role of Abeta plays in Alzheimer's disease, they said.

"Understanding how the brain protein Abeta causes nerve cell death in Alzheimer's patients is key if we are to find a cure for this disease," said Karen Marshall from University of Sussex.

"Our study clearly shows that the aggregation of Abeta into bigger species is critical in its ability to kill cells. Stopping the protein aggregating in people with Alzheimer's could slow down the progression symptoms of the disease. We hope to work towards finding a strategy to do this in the lab and reverse the damaging effects of toxic Abeta," she said.

"This is a really exciting new tool that will contribute to research to uncover the causes for Alzheimer's disease and enable tangible progress to be made towards finding targets for therapy," added Louise Serpell from University of Sussex.

The findings were published in the journal Scientific Reports. 

 this is only for your information, kindly take the advice of your doctor for medicines, exercises and so on.
https://gscrochetdesigns.blogspot.com. one can see my crochet creations
https://gseasyrecipes.blogspot.com. feel free to view for easy, simple and healthy recipes

https://kneereplacement-stickclub.blogspot.com. for info on knee replacement

Common antidepressant may halt plaque growth associated with Alzheimer’s

New research published in the journal Science Translational Medicine reveals that the frequently prescribed antidepressant citalopram, also known as Celexa, could play a role in halting the progression of the brain-wasting disease.

Antidepressants like citalopram offer hope by targeting the brain’s amyloid beta proteins, which seem to be responsible for triggering the plaque build-up associated with the decline of memory and cognitive function in Alzheimer’s patients.

“The way the Alzheimer’s field is going is [we are] trying to find the initial insult in Alzheimer’s disease,” study a Dr. “We think it is the build-up of this amyloid beta peptide, and once it builds up, a lot of things go wrong.”

Amyloid beta proteins are produced by normal brain activity, but in Alzheimer’s patients, levels of this protein increase abnormally, clumping together to form plaques.

Previous research has shown that serotonin, a brain chemical thought to influence mood, seems to reduce amyloid beta production in the brain. In fact, an earlier study demonstrated that people with a history of antidepressant use had less amyloid plaques in their brains than those who never used antidepressants.
A popular type of antidepressant known as selective serotonin reuptake inhibitors (SSRIs) can influence serotonin levels, so the researchers were interested in testing its effects on mice and human models.  Using mice genetically engineered to develop Alzheimer’s disease, the researchers discovered that the SSRI citalopram was able to completely stop the growth of brain plaques in the study group.

“SSRIs, by lowering a-beta levels 25 percent, were able to completely block that [plaque] growth,” Cirrito said. “The plaques never got smaller, and we couldn’t reverse the plaque [that was already there], but we could prevent it from growing.”

The researchers also tested citalopram in a group of cognitively healthy young adults. They discovered that after receiving a single dose of the antidepressant, the participants saw a 37 percent reduction of amyloid beta levels in their cerebrospinal fluid.
Currently, Cirrito said amyloid beta has no “known function” in the human body, and decreasing levels of the protein in humans doesn’t seem to have any ill effects on health. However, he noted that much research needs to be done before SSRIs can be proven effective at treating or preventing Alzheimer’s in humans.

“The SSRIs in this study were all given to healthy young people not at risk for Alzheimer’s,” Cirrito said. “We don’t know if the same thing will happen in people older, and not at risk for Alzheimer’s, and have no idea if it affects cognition,” Cirrito said.

Furthermore, he cautioned people against preemptively taking SSRIs in hopes of fending off or treating Alzheimer’s disease.
“There are certainly side effects [of SSRIs] that if they don’t need to be taken, it’s not a good idea to be on them until we know they can have an effect on Alzheimer’s, it’s premature to take them as a preventative measure,” Cirrito noted. “We’ve cured a mouse of a lot of different diseases, including Alzheimer’s disease many times, and those things haven’t panned out in people yet.”

Next, Cirrito and his team hope to move forward to study how SSRIs act on the brain to lower amyloid beta levels – and to continue to study the effects of SSRIs on different human populations.  

“On the human side, we’re doing a similar study to what we just completed but in people [who are] older and at risk for Alzheimer’s, to see if we can affect a-beta in those people or not,” Cirrito said. “If not, then the utility of this for people with Alzheimer’s would go down dramatically.” 

PS- THIS IS ONLY FOR INFORMATION, ALWAYS CONSULT YOU PHYSICIAN BEFORE HAVING ANY PARTICULAR FOOD/ MEDICATION/EXERCISE/OTHER REMEDIES.

PS- THOSE INTERESTED IN RECIPES ARE FREE TO VIEW MY BLOG-

HTTP:GSEASYRECIPES.BLOGSPOT.COM/

FOR INFO ABOUT KNEE REPLACEMENT, YOU CAN VIEW MY BLOG-

HTTP://KNEE REPLACEMENT-STICK CLUB.BLOGSPOT.COM/

FOR CROCHET DESIGNS

HTTP://MY CROCHET CREATIONS.BLOGSPOT.COM