There is currently no cure for Alzheimer's disease, but there may yet be hope of reversing the symptoms of the neurodegenerative disease if a certain prototype cognitive helmet designed by Dr. Gordon Dougal of the University of Sunderland lives up to its creator's and its user's expectations. More details on this strange-looking helmet after the jump.

In a new study done, a therapeutic molecule was administered to the spine and marked improvements in Alzheimer's disease appeared within a short span of time.

The study used Etanercept to lower a substance that has the ability to interfere with the neural impulses in the brain when it reaches excess amounts. Details of the study can be found in the full article.

There is now a new ray of hope shining on science and those searching for cures to the most incurable diseases. Cedars-Sinai Medical Center's researchers from the Board of Governors Gene Therapeutics Research were able to find a way to sustain gene therapy for longer periods of time, without having to alert the body's innate immune system and ending the gene therapy.

Through a demonstration using an animal specimen, researchers were able to show that gene delivery using HC-Adv adenoviral vectors were able to completely bypass the immune system. The researchers said that this manner of gene therapy delivery is safer as well as effective compared to existing methods.

This method of gene therapy aims to cure diseases such as Parkinson's, Alzheimer's, as well as Multiple Sclerosis. Other gene therapies, such as the use of genetically-modified blood cells, have been developed to cure severe diseases.

Researchers from Stanford University have developed a blood test that appears to identify patients who have or are prone to contracting Alzheimer's disease. If the initial findings prove correct, then doctors will have a new tool in diagnosing this neurodegenerative disease which kills 66,000 Americans each year.

The scientists have found that those with Alzheimer's consistently have a set of 18 distinct chemical signals in their blood. Stanford neurology Professor Tony Wyss-Coray, the team leader of the project, said that these are signaling proteins that cells use to communicate with each other and that they decided to look for the more distinctive proteins in Alzheimer's patients.

In one of their experiments, the scientists found that the new method was able to correctly identify Alzheimer stricken individuals 90% of the time. The test was also able to classify individuals without Alzheimer's disease but had other mild cognitive diseases with 87% accuracy.

While the results look promising, Wyss-Coray said that it will take at least two more years and further studies before this new method can be adopted by clinics across the United States. If this is further developed, then this will be another new tool in the fight against Alzheimer's disease.

New findings have revealed that the memory-losing disease, Alzheimer's, is actually a form of diabetes. Northwestern University scientists have discovered that the toxic protein "amyloid ß-derived diffusible ligand" - or ADDL - takes away the insulin receptors from the nerve cells, thereby making them insulin resistant.

Hampering insulin and its receptors to the brain results to memory loss as the two are key components in memory formation. Now having determined that Alzheimer's may be caused in part by this insulin resistance, thanks to the attack of ADDL, the next question to confront then would be how this attack is triggered.

Weinberg College's William L. Klein, leader of the research, explains:

We think this is a major factor in the memory deficiencies caused by ADDLs in Alzheimer's brains. We're dealing with a fundamental new connection between two fields, diabetes and Alzheimer's disease, and the implication is for therapeutics. We want to find ways to make those insulin receptors themselves resistant to the impact of ADDLs. And that might not be so difficult.

The discovery is published online by the FASEB Journal.

Another gene linked to Alzheimer's disease has been found. Early this year, the gene SORL1 was discovered to be a factor in late-onset dementia, along with ApoE4. Scientists have found another clue to the mind degenerating disease.

According to journal Neuron, people with a damaged copy of the GAB2 gene are more susceptible to developing Alzheimer's in their later years. Late onset Alzheimer's hit one out of ten people over 65 and about 50 percent of people over 85. Researchers from the Institute of Neurology and other institutions studied DNA gathered from 1,411 people and found that GAB2 has an effect on ApoE4.

People with Alzheimer's commonly have protein "tangles" in their brains. It was found that GAB2 (if undamaged) stops a protein called tau that has a direct effect on the formation of the said tangles. So if a person has a bad copy of GAB2, tau runs amok and you know what happens next. Alzheimer's Society's director of research, Professor Clive Ballard had this to say:

This impressive research suggests a common gene could be responsible for a four-fold increased risk of developing Alzheimer's disease. It is the most important risk factor gene to be identified in relation to tangles, which develop in the brain in Alzheimer's disease.

Interesting discovery. The faster they discover things, the faster they find cures, right? Let's hope they do.

Although it's not supposed to give anyone ideas for human testing, a report by Reuters had announced that scientists had found a way to switch off certain genes related to Alzheimer's disease. They found out that by turning off a certain gene, called Cdk5, they were also able to make experimental mice smarter.

These researchers were in the process of finding a cure for memory problems, when they stumbled upon genetic engineering techniques that would allow them to switch certain genes on and off.

Cdk5, a gene that determines the production of an enzyme that is reputably linked to Alzheimer's, was one of those that they could turn off.

And what's more, the mice that did have Cdk5 turned off became better at tasks based on associated learning. Dr. James Bibb of the University of Texas Southwestern Medical Center said, "It's the most important kind of learning in the animal kingdom. It's how we know where our car is and that is our wife or our husband and that's our kids. It's how we connect things."

When placed inside a maze together with ordinary mice, the altered mice performed much better in contrast. "The increase in sensitivity to their surroundings seems to have made them smarter. It was very clear right off the bat that the loss of Cdk5 made them have a much stronger associative memory," said Bibb.

 

The PS3's launch in Europe has been hailed by Gamestation as a "success", and although eBay sales aren't going down amazingly well at the moment, what Sony's PS3 lacks in auction fever it makes up in curing diseases all over the world. That's right, we aren't talking about a game like Call of Duty - we're talking about the PS3's involvement in curing Alzheimer's disease with Stanford University's Folding@Home project.

You've probably seen our call for PS3 users to unite and join the QJ.Net Folding@Home Team, but basically what it does is use your PS3's idle CPU while investigating protein folding which has been thought to be the root of diseases such as Alzheimer’s Disease, Parkinson’s Disease, cystic fibrosis, Huntington's Disease, and some types of cancer. You may ask why we're posting this once again, but this isn't just an appeal to ask you to join.

The PS3 has already made a significant impact on the Folding@Home, with PS3s providing 346 Teraflops of their CPU power, close to triple of what all Windows PCs running the program and 100 more TFLOPs than Windows, Mac, Linux, GPU, and other Operating Systems put together. We would like to thank everyone on the QJ.Net Folding@Home team who have joined since our last post and have helped the PS3 achieve this great feat. QJ's Folding@Home team stats can be viewed here.

 

So as you can see, the PS3 really is making a difference. You may think that your PS3 won't be responsible for curing a disease, but think about it: your PS3 has over 10 times the TFLOPS (processing power) of the average computer - put it to good use. Who knows, the PS3 could be the thing that cures a disease such as Alzheimer’s once and for all. Even if you don't have a PS3 yet, it's quite cool to know that a console you support is giving something back to the world.

If you have just got a PS3 from Europe or another part of the world and would like to donate your processing power to a good cause, click here to learn more about how to join the QJ.Net Folding@Home team. Even if you don't have your PS3 yet, you can download the Folding@Home application to your PC too, it just won't be as effective as the Cell-powered PS3. But you're still helping.

Scientists have discovered that the gene SORL1 - the fifth gene to be linked to Alzheimer's - can identify whether a person may develop Alzheimer's disease in their later years. SORL1 and ApoE4 are the only two genes that have been identified to have abnormalities on people with late-onset Alzheimer's.

Although the time span between discoveries is daunting (ApoE4 was discovered in 1993, SORL1 was discovered early 2007), it's still a good step toward preventive medicine. Now scientists have one more ace up their sleeve to find out how they can prevent the disease that plagues a good portion of older folk.