Study uncovers link between Alzheimer's and Parkinson's

Scientists have discovered biological mechanisms that may link Parkinson's disease to Alzheimer's disease, according to a study published in the journal Acta Neuropathologica.

Researchers from the University of Florida say their findings could lead to targets for new treatment that combats both Alzheimer's and Parkinson's disease, as well as many other neurological disorders.

For their study, the researchers investigated a protein called tau. They explain that tau is a soluble protein in the brain that binds to microtubules - components that play an important part in cell processes - helping to support neuronal function.

The normal function of tau is supported by phosphorylation - a process that switches protein enzymes on and off and regulates their function and activity.

However, the researchers say that in some diseased brains, the tau protein can become abnormally phosphorylated and cause "clumps" or "tangles." These tangles, called tauopathies, are linked to cognitive impairment found in some neurodegenerative diseases, such as Alzheimer's, and are also linked to around 20% of Parkinson's cases.

LRRK2 'phosphorylates tau protein'

Parkinson's patients can develop tangles of the tau protein as a result of a mutated enzyme called LRRK2, the researchers say.

From conducting a series of mammalian studies, the researchers discovered that standard LRRK2 adds groups of phosphate to tau protein, while mutated LRRK2 adds significantly more phosphates to tau protein.

Using these findings, the research team were able to uncover two sites on the tau protein - T149 and T153 - where the mutated LRRK2 was able to add phosphate groups, which they linked to tangle formations.

The researchers then went on to test their findings on human brain tissue. From this, they discovered that the two sites previously identified on the tau protein that were targeted by LRRK2, were altered the same way in human tissue with LRRK2 mutation.

When testing this finding on human brain tissue that was affected by Alzheimer's disease, and other neurodegenerative diseases that form tangles, they found these alterations were the same.

Explaining their findings, the researchers say:

"Our data, in aggregate, demonstrate that LRRK2 directly phosphorylates tau at T149 and T153 in vitro and the ability of LRRK2 to phosphorylate tau at these sites may underlie its ability to promote tauopathy in our novel mouse model.

Our current in vivo studies are the first of their kind and provide compelling evidence that LRRK2 and tau interact in a disease-relevant manner."

Potential for therapeutic targets

The researchers add that their findings have the potential to provide new therapeutic targets for both Alzheimer's and Parkinson's disease.

"Until now, nobody has really understood what the overlap between Alzheimer's and Parkinson's disease was, or if it were important," says Jada Lewis, associate professor of neuroscience at the Centre for Translational Research in Neurodegenerative Disease at the University of Florida. "Our study ties these diseases together in a unique way."

The researchers conclude that their findings show that LRRK2 genetic studies in human tauopathies may be warranted.

Medical News Today recently reported on a study suggesting that exercise may ward off Alzheimer's and Parkinson's disease.

Written by Honor Whiteman

Copyright: Medical News Today 

Article c/o: http://www.medicalnewstoday.com/articles/267885.php

Early Balding May Be Linked With Lou Gehrig's Disease

Men who show signs of early balding may be at an increased risk of the rare but incurable disease amyotrophic lateral sclerosis (ALS), also called Lou Gehrig's disease, a new study finds.

The link between the two conditions may provide a new direction in investigating the poorly understood neurodegenerative condition, the researchers said.

The researchers looked at more than 50,000 men ages 46 to 81, and asked them to recall the shape of their hairline at age 45, and choose from a series of pictures depicting no balding, moderate or extensive balding.

Nearly 44 percent of men reported no balding, about 42 percent of men reported moderate balding and 14 percent reported extensive balding at 45 years old.

Sixteen years later, 11 of 5,500 men who had reported extensive balding were diagnosed with ALS, while 13 of 17,500 men with no balding were affected by the disease. The researchers calculated that men with extensive early balding were about three times as likely to develop ALS, compared with men who hadn't lost hair early in life.

The researchers said their results should be interpreted cautiously until the link between early balding and ALS is confirmed in future studies.

"This doesn't mean that bald people should worry," said study author Elinor Fondell, researcher at Harvard School of Public Health. Moreover, the link may not be true for everyone there were 11 people diagnosed with ALS who didn't have early balding, Fondell noted.

A mysterious disease

ALS is a disease of the nerve cells in the brain and spinal cord that control muscle movement. The early symptoms of the condition usually include weakness and shrinking of muscles, and as the condition progresses, patients develop disabling movement problems, and ultimately cannot breathe on their own.

About 5,600 people in the United States are diagnosed with ALS each year, according to the ALS Association. Men are at higher risk for ALS than women. Half of people affected by the disease live more than three years after diagnosis, but less than 10 percent of patients live more than 10 years after diagnosis.

"We know very little about what causes ALS, and there's only one approved drug that prolongs life, for about three months," Fondell said.

"If the link between early balding and ALS can be confirmed in other populations, and if other researchers look at this on a molecular level and see if there's some basis to this, then that in the future may lead to new drugs for ALS," she said.

Men in the study with moderate early balding had a 50 percent higher risk of ALS compared with men with no balding. The results showed a clear trend: with increasing levels of balding at age 45, the risk of ALS increased, the researchers said.

The results were controlled for potential risk factors of both early balding or ALS, such as smoking, weight, as well as vitamin E intake, which may protect against ALS.

What may underlie the link

One possible mechanism for a link between ALS and early balding may involve a protein called the androgen receptor, a protein that regulates the hormone testosterone and has been shown to be associated with an increased risk of early balding.

In 1980, researchers proposed the possibility that androgen receptor is involved in ALS. The idea originated when researchers observed that the disease affected all motor neurons except those that lacked the androgen receptor.

"Everybody got so excited about this theory," Fondell said. "So they tested it, but found that the androgen receptor does work," so the idea wasn't pursued further.

"I think they dropped it too early," Fondell said.

Another possible explanation could involve a genetic variation in early balding recently identified in an analysis of genetic studies of the condition. The variation is in a gene located close to another gene that has been implicated in ALS. Given the physical proximity of the two genes, it is possible that one affects the other, the researchers said.


The study was published Aug. 13 in the American Journal of Epidemiology.

Read more: http://www.foxnews.com/health/2013/08/23/early-balding-may-be-linked-with-lou-gehrig-disease/#ixzz2dTnrvd6d

Omega-3 Fatty Acids Improve Recovery

A popular omega-3 fatty acid with an ingredient in curry spice may offer millions of seniors 
some relief from spinal damage, research reveals. Cervical Myelopathy is the most common 
spine-related walking problem for people over 55, and it can lead to disabling neurological 
symptoms, such as difficulty walking, neck and arm pain, hand numbness and weakness of the 
limbs.

 UCLA researchers’ findings suggest that the two supplements help repair nerve cells 
and maintain neurological function after degenerative damage to the neck. 

 DHA is an omega-3 fatty acid shown to repair damage to cell membranes. Curcumin is 
a compound in turmeric, an Indian curry spice, and a strong antioxidant that previous 
studies have linked to tissue repair. Both reduce inflammation.

 “Our findings suggest that diet can help minimize disease-related changes and repair 
damage to the spinal cord,” said principal investigator Dr. Langston Holly, associate 
professor of neurosurgery at the David Geffen School of Medicine at UCLA.

The supplements might do the trick for those who are afflicted with back pain, but your 
readers also should know that support at home from a Home Instead CAREGiverSM could 
help, too.

What Is Your Risk Of Developing Alzheimer's?

Despite fears of Alzheimer’s, many would like to know their risk for the disease

Alzheimer’s disease can’t be prevented or cured, and it ranks second only to cancer among diseases that people fear. Still, in an international study last year from the Harvard School of Public Health, about two-thirds of respondents from the United States said they would want to know if they were destined to get the disease. Although there are no definitive tests that predict whether most people will get the disease, people sometimes want such information for legal and financial planning purposes or to help weigh the need for long-term-care insurance.

Current tests to identify the risk of developing Alzheimer’s disease when no symptoms are present provide only limited information, and health insurance generally doesn’t cover them. But that’s not stopping some people from trying to learn more.

Most of the 5 million people who have Alzheimer’s developed it after age 60. In these cases, the disease is likely caused by a combination of genetic, lifestyle and environmental factors. About 5 percent of Alzheimer’s patients have inherited an early-onset form that is generally linked to a mutation on one of three chromosomes.


Research suggests that the brain may show signs of Alzheimer’s decades before obvious symptoms appear. Scans can identify the presence of beta-amyloid, a protein that is often deposited in the brains of people with the disease, for example. Changes in proteins in the blood or cerebrospinal fluid may also be associated with Alzheimer’s disease.

But tests to measure these changes are available only in a research setting, and insurance typically doesn’t cover them. James Cross, head of national medical policy and operations for Aetna, says his company “does not consider blood tests or brain scans medically necessary for diagnosing or assessing Alzheimer’s disease in symptomatic or asymptomatic people because the clinical value of these remains unproven.”

Genetic testing is somewhat easier to arrange, but insurers generally won’t pay for it, either.

In addition, genetic counselors caution that long-term-care insurers may use genetic testing results when evaluating whether to issue a policy. The Genetic Information Nondiscrimination Act prohibits health insurers and employers from discriminating against people based on their genetic information. However, life and long-term-care insurers are not covered by the law.

“Before anyone has genetic testing, they should get life insurance and long-term-care insurance,” says Jill Goldman, a certified genetic counselor at the Taub Institute at Columbia University Medical Center.

Genetic testing for late-onset Alzheimer’s involves one gene, the apolipoprotein E (APOE) gene on the 19th chromosome. The gene comes in three different forms — E2, E3 and E4. Everyone inherits one form, or allele, from each parent. Having one or two of the E4 variants can increase a person’s risk of developing Alzheimer’s disease three to 15 times.

About half of those who develop late-onset Alzheimer’s, however, don’t have any E4 alleles at all. Genetic testing in asymptomatic people therefore isn’t definitive or even all that informative, say experts. For late-onset Alzheimer’s, “the predictive value of genetic testing is low,” says Mary Sano, director of the Mount Sinai Alzheimer’s Disease Research Center.

But sometimes people want information, even if it’s inconclusive.

Brian Moore, whose father died of Alzheimer’s at age 89, wanted to know more about his genetic risk for the disease. Moore, 48, was better equipped than most to understand the testing: A neuropathologist who co-chairs the department of pathology at Southern Illinois University’s School of Medicine, he has performed hundreds of autopsies on the brains of people who died of Alzheimer’s disease.

Moore contacted 23andMe, a company that for $299 offers a genetic analysis of a person’s risk for more than 100 diseases and conditions, including Alzheimer’s, based on the APOE gene. The company sent him a specimen kit with a container for saliva collection that he then sent to a lab for analysis. About six weeks later, he logged on to the company’s Web site and learned that he has two E3 alleles, the most common variants, which means that his Alzheimer’s risk is average, at least as it relates to the APOE gene.

“It was reassuring,” he says. “I know it’s not determinant, and environment and lifestyle also play a role. But at least I have that base covered.”

The National Society of Genetic Counselors and the American College of Medical Genetics practice guidelines recommend against direct-to-consumer APOE testing for late-onset Alzheimer’s, in part because of the difficulty of interpreting the results.

Ashley Gould, 23andMe’s vice president of corporate development and chief legal officer, says that if people want help understanding their results, there are genetic counselors they can speak with. This service is available by phone for a fee based on the level of service.

But in the case of the APOE gene, some experts say, the information isn’t all that helpful.

“The things we know that really impact the disease are related to lifestyle,” says George Perry, dean and professor of biology at the University of Texas at San Antonio, who is the editor-in-chief of the Journal of Alzheimer’s Disease. “Be mentally and physically active, eat a diet rich in fruit and vegetables. These reduce the risk of developing the disease by at least half.”

This column is produced through a collaboration between The Post and Kaiser Health News. KHN, an editorially independent news service, is a program of the Kaiser Family Foundation, a nonpartisan health-care-policy organization that is not affiliated with Kaiser Permanente. E-mail: questions@kaiserhealthnews.org.

Article c/o:  http://www.washingtonpost.com

Scientists See Progress In Alzheimer's Despite Growing List of Drug Failures

Another once-promising Alzheimer's drug has just been tossed on the pharmaceutical scrap heap.

This time it's a drug called bapineuzumab. Like several previous experimental drugs, it was designed to attack the plaques that build up in the brains of people with Alzheimer's.

And like those earlier drugs, it failed.

The drug company Pfizer issued astatement yesterday saying a study of about 1,300 patients with mild-to-moderate Alzheimer's disease found that bapineuzumab didn't help. Pfizer also announced it was discontinuing all studies of the intravenous form of the drug.

The failure of bapineuzumab is the latest evidence that treating Alzheimer's may not be as simple as going after plaques in the brain.

But scientists remain confident that treatments will need to target the major component of those plaques, a protein called amyloid beta or "A-beta."

"It all begins with A-beta," Robert Vassar, an Alzheimer's researcher at Northwestern University, tells Shots. "If we could limit the production of A-beta in the brain or enhance its clearance out of the brain then I think we could really make some headway in terms of preventing Alzheimer's disease and perhaps curing it."

The question is whether it makes sense to attack the A-beta in plaques that have already formed.

Recently, some scientists have suggested that the sticky plaques actually protect the brain by trapping bits of A-beta. These scientists suspect that it's free-floating particles of A-beta that actually damage brain cells.

If that's the case, drugs would have to eliminate free floating bits of A-beta, not just the A-beta in plaques.

One way to accomplish this may be to interrupt the process that forms A-beta in the first place, researchers say.

Several drugs designed to do this are in the pipeline. And their prospects are looking bright after a study found that people with a gene mutation that reduces A-beta production were much less likely to develop Alzheimer's.

The failure of plaque-attacking drugs may also be a sign that treatments need to begin well before people begin showing symptoms of Alzheimer's.

"My opinion and the opinion of many colleagues is that once the A-Beta begins to accumulate in the brain and a person actually has memory symptoms it may actually be too late," Vassar says.

And ultimately, treating Alzheimer's may require going after A-beta in several different ways, says William Mobley, chairman of the department of neurosciences at the University of California, San Diego. That could mean finding a way to both reduce production of A-beta and remove it from the brain, he says.

"Several shots on goal may be needed," Mobley says.

Article care of : http://www.npr.org