Gene mutation will help Alzheimer's treatment

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Connie K. Ho for redOrbit.com – Your Universe Online

5 million. That’s the number of people in the U.S. suffering from Alzheimer’s disease, according to a recent CNN article. Scientists recently announced that they had discovered a gene that fights Alzheimer’s. This is a positive step forward as the gene could help develop treatments to fight the disorder.

In the journal Nature, researchers explained how the gene that caused an early form of Alzheimer’s could also be created to produce an office effect, prohibiting the development of the disorder. According to the Guardian, carriers of the mutation have a 47% greater likelihood of living until 85 years of age as compared to those who don’t have the mutation. The findings also discuss how new drugs could copy the effect of the mutation.

“Less than 1% of the population has these alleles,” explained Dr. William Thies, chief medical and scientific officer of research and advocacy group Alzheimer’s Association, in a Reuters Health article. “But many companies are working on compounds that target the mechanism they found and so might be encouraged by these results.”

Alzheimer’s is a common form of dementia and early signs include memory loss, mood swings, as well as feelings of isolation and withdrawal. The illness is progressive and those who are diagnosed with the disorder become dependent on others to help them with daily tasks. With Alzheimer’s disease, the brain is plagued with sticky plaques made of amyloid beta, a peptide. The amyloid beta is from the amyloid precursor protein (APP), which is a larger protein. Scientists have discovered about two dozen mutations in the APP genes that lead to early-onset Alzheimer’s within the last twenty years. Early-onset Alzheimer’s is normally diagnosed in people who are a bit younger than 65.

However, researchers from deCODE genetics in Iceland found that a new mutation in the APP gene does the opposite and has certain benefits. In the project, scientists sequenced the genomes of 1,795 Icelanders. It led to the discovery that participants of 85 years of age and older who had the beneficial mutation had a 81 percent less likelihood to develop Alzheimer’s when compared to others in the same group. In all age groups, those who had the variant genes were four times less likely to develop the neurogenerative disease.

“It confers extraordinarily strong protection,” noted lead scientist Dr. Kari Stefansson. “We found only five Alzheimer’s cases (out of thousands of people) with it.”

As well, the mutation is so rare that its discovery will help scientist in creating drugs that can prevent or treat Alzheimer’s. The mutation influences how APP is broken up and, after the brain produces the protein, the enzymes are broken into pieces. The enzymes are listed as alpha, beta, and gamma. The break up of APP by Alpha-secretase makes it so amyloid beta and plaques cannot be produced. As such, the fragment allows for growth and survival of the neurons.

On the other hand, the beta-secretase (BACE) works with the gamma-secretase to cut APP, so it can produce amyloid beta. The BACE then adheres to other amyloid beta fragments and forms plaques. Luckily, the beneficial mutation can stop the BACE’s ability to cut the APP and reduces the creation of amyloid beta by 40 to 50%t. Overall, it slows down the production of BACE, which hinders Alzheimer’s from developing.

A number of follow-up studies also showed that the DNA sequence with the mutation shielded the participants from decline in brain performance that is normally related old age. It proves that Alzheimer’s and other age-related neural problems are connected to a cycle of disorders and have the same basic cause.

“This gives you a proof of concept that if you inhibit BACE it will protect against Alzheimer’s,” remarked Stefansson in the Reuters Health article. “Big pharma has been working on inhibitors for beta-secretase for 15 to 20 years, and this offers greater confidence” that those efforts will pan out.”

According to Reuters Health, many companies are working on creating commands that can stop BACE actions.  For example, Merck presented early-stage human trails of MK-8931 last April. Vitae Pharmaceuticals and Boehringers Ingelheim are also working together to create a BACE inhibitor. Likewise, Eli Lilly and Co’s BACE inhibits is already in mid-stage human trials. However, it’ll mostly take at least four to five years or longer until the drugs become successful treatments.

“We know that the development of Alzheimer’s can be linked to a combination of genetic and lifestyle factors. We still have a lot to learn about what happens in the brain but this research offers new insight into a gene we already know is linked to the disease,” Anne Corbette of the Alzheimer’s Society told  HYPERLINK “http://www.guardian.co.uk/science/2012/jul/11/rare-genetic-mutation-alzheimers” the Guardian. “One in three people over 65 will develop dementia. This development offers interesting new information about how our genes might affect our chances of developing Alzheimer’s disease. It could also provide a new target for future investigations to find treatments to help people live well with dementia, or even find a cure.”

Source: Connie K. Ho for redOrbit.com - Your Universe Online

Source: redOrbit (http://s.tt/1hLVD)

Abnormal Protein May Explain Loss of Smell With Alzheimer’s

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The protein kills nerve cells in the nose, animal study finds.

(HealthDay News) -- A loss of a sense of smell can be one of the earliest signs of Alzheimer's disease.

New research suggests that an abnormal form of a protein -- amyloid precursor protein, or APP -- which has been previously associated with the Alzheimer's disease may be to blame.

A study in mice found that animals genetically engineered to produce high levels of the abnormal protein experienced high levels of death in nerve cells in their nose compared to normal mice.

Researchers say the findings may explain why people suffering from the progressive illness often lose their sense of smell while the disease is still in its initial stages. They added this new insight might help doctors detect the condition early on.

"Deficits in odor detection and discrimination are among the earliest symptoms of Alzheimer's disease, suggesting that the sense of smell can potentially serve as a canary in the coal mine for early diagnosis of the disease," study leader Leonardo Belluscio of the U.S. National Institute of Neurological Disorders and Stroke, said in a news release.

"The changes taking place in the olfactory system as a result of Alzheimer's disease may be similar to those in other regions of the brain but appear more rapidly," he added.

APP has been detected in the nose nerve cells of some people with early onset Alzheimer's, a rare form of the disease that runs in families and strikes before age 65.

The researchers found mice making the mutated form of APP had four times as much olfactory nerve cell death at three weeks of age than normal mice.

When researchers blocked the production of high levels of the mutated protein, more olfactory nerve cells survived.

"Reducing APP production suppressed the widespread loss of nerve cells, suggesting that such disease-related death of nerve cells could potentially be stopped," explained Belluscio.

The study, published in the Sept. 28 issue of The Journal of Neuroscience, also found that the cells that died in the nose did not contain amyloid plaques, which are derived from APP. Plaques have long been believed to contribute to the death of nerve cells in the brains of people with Alzheimer's, leading to memory loss.

The researchers say the findings suggest that APP itself may be responsible for the death of nerve cells.

"Together, these results support the hypothesis that amyloid proteins are involved in the degeneration of the brain that occurs with Alzheimer's disease," Donald Wilson of New York University School of Medicine and the Nathan Kline Institute for Psychiatric Research, said in a news release from the journal.

"Further, they provide an exciting opportunity to explore how to prevent or reverse the events that lead to cell death and, ultimately, dementia," added Wilson, an olfactory system expert who was not involved in the study.

While more research is needed, it should be noted that studies involving animals often fail to produce similar results with humans.

More information

The National Institutes of Health provides more information on Alzheimer's disease.

SOURCE: Society for Neuroscience, news release, Sept. 27, 2011

Protein linked to Alzheimer's disease doesn't act alone

EurekAlert

Karen Mallet


GUMC researchers find APP needs to work with 'Reelin' protein to maintain healthy communication between brain neurons

Washington, DC – A team of U.S. investigators led by neuroscientists at Georgetown University Medical Center (GUMC) are steadily uncovering the role that amyloid precursor protein (APP) - the protein implicated in development of Alzheimer's disease - plays in normal brain function. In the June 10 issue of the Journal of Neuroscience, they discovered that APP interacts with another protein known as Reelin to promote development of abundant connections between brain neurons.

Reelin, named for mice that "reel" around when they don't have the protein, has been thought to be involved in stimulating growth of neuronal dendrites – the branching projections that transmit signals to other neurons. It also has been implicated in some brain disorders, but up until now, little was known about how Reelin interacts with APP.

Researchers say that showing that APP and Reelin work together doesn't have immediate implications for therapeutic treatment of Alzheimer's disease in humans, but they say the work helps provide the background necessary to understand finally why a brain veers toward the progressive memory loss seen in this devastating disease, which impacts 5.3 million people yearly in the U.S..

"In the last 20 years we have made tremendous progress in understanding how APP can become toxic. But I think the flip side is equally interesting: Why does APP even exist in the brain? We are only now just beginning to figure that out," says the study's senior author, G. William Rebeck, PhD, associate professor in the Department of Neuroscience at GUMC.

What has long been known is that mutations in the gene that produces..........read the whole article

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Study suggests how Alzheimer's attacks brain

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US scientists proposed a new theory of how Alzheimer's disease kills brain cells they said opens new avenues of research into treatments for the fatal, brain-wasting disease.

They believe a chemical mechanism that naturally prunes away unwanted brain cells during early brain development somehow gets hijacked in Alzheimer's disease.

"The key player we're focusing on is a protein called APP," said Marc Tessier-Lavigne, executive vice president of research drug discovery at the US biotechnology company Genentech Inc , whose study appears in the journal Nature.

Tessier-Lavigne said amyloid precursor protein, or APP -- a key building block in brain plaques found in Alzheimer's disease -- is the driving force behind this process.

"We know that APP is...read the whole article

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