Jul 132010

– When Combined with a Known Alzheimer’s Gene, Your Alzheimer’s Risk may be Doubled –

A gene known as FTO, which appears to be correlated with obesity in humans, may also increase risk of Alzheimer’s disease and dementia, according to new research presented today at the Alzheimer’s Association International Conference on Alzheimer’s Disease 2010 (AAICAD 2010) in Honolulu, HI. And when a person has certain variants of both FTO and a recognized Alzheimer’s risk gene known as APOE, the risk of Alzheimer’s could be doubled.

“While scientists know Alzheimer’s involves progressive brain cell failure, they have not yet identified any single reason why cells fail,” said Maria Carrillo, Ph.D., senior director of Medical and Scientific Relations at the Alzheimer’s Association. “However, there is evidence about certain factors that may increase the likelihood of developing Alzheimer’s.”

“Some of these factors we can’t control, such as age, family history, and genetics,” Carrillo said. “Others we may be able to influence, including heart health, tobacco and alcohol use, and head injury.”

FTO has previously been shown to affect body mass index (BMI), leptin levels (a protein hormone that plays a key role in appetite and metabolism), and the risk for diabetes. These vascular risk factors have also been associated with risk of Alzheimer’s disease.

In the study reported at AAICAD 2010, Caroline Graff, M.D., Ph.D., and colleagues at the Karolinska Institutet, Sweden, explored the direct role of the FTO gene on Alzheimer’s and dementia risk in old age. In addition, a possible interaction of FTO with the APOE gene, a well-established genetic risk factor for Alzheimer’s, was assessed. The researchers followed 1,003 people aged 75 years and older without dementia from the Kungsholmen project, Sweden, for nine years to detect new cases of Alzheimer’s and dementia. All participants had been genotyped for FTO and APOE on DNA sampled at the beginning of the study.

They found that people in the study population who carried the AA gene-variant in the FTO gene had a 58 percent increased risk for developing Alzheimer’s and a 48 percent increased risk for developing dementia compared with those who did not have this genetic variant, after adjustment for age, gender, education, and APOE genotype.

The findings also suggest that the risk-effect of FTO-AA on dementia is further elevated to 100 percent increased risk in the presence of APOE ε4, which is the highest risk variant of the APOE gene. The effect of the FTO-AA genotype on Alzheimer’s and dementia risk remained after additional adjustment for diabetes, BMI, cardiovascular disease and physical inactivity.

“One of the intriguing aspects of the results is that the increased risk was independent of the traits previously associated with FTO, such as obesity and diabetes measured at baseline,” Graff said. “Our results suggest that the mechanism by which FTO is associated with an increased risk for Alzheimer’s and dementia may be different from how it increases the risk for obesity.”

“This is a fascinating early finding, which fits with the known connections between heart health and brain health,” Carrillo said. “However we do need to see these results confirmed by other researchers. In fact, we desperately need to know more, in general, about the genetics and other causes of Alzheimer’s so that we have additional targets for therapies and preventions. One major positive step in that direction would be for the federal government to address its chronic underfunding of Alzheimer’s disease research.”

Please visit alz.org for more information.

  3 Responses to “New Study: A Gene Known as FTO, Which Appears To Be Correlated With Obesity in Humans, May Also Increase Risk of Alzheimer’s Disease and Dementia”

  1. My father was digonased with vascular dementia some 3 years ago and it has progressed to the stage where he is now in a wonderful care home. When he was obviously getting worse a friend suggested joining her in attending a course of 6 weeks which was run by the Alzheimers Society. We duly went along and it was the biggest learning curve I have had for some time. Alan, the gentleman who taught’ us was a wonderful, compassionate and caring man and answered all of our questions very patiently. My father was taken too hospital during this time and was there for nearly 4 weeks, whilst he was there it occurred to me that even some healthcare professionals have no idea how to handle people with dementia. All professionals should be asked to complete a course of this subject. I have learned that it is pointless asking someone with dementia a question because it just confuses them more and they can get very upset. I try very hard not to ask my father any questions, I just make statements, wjen I arrive I tell him what the weather is like outside rather than ask how he is. I don’t ask him if he wants a drink I just tell him I am having one and I will bring him one too. He likes to talk about his work and I just let him get on with it and say what I think is the right thing in the right space and he is happy in himself with that. People in general are frightened of anyone who is not the norm’ and I think that they should be educated noto to be. I hope that in some small way I can do my bit for those with dementia by trying to educate the people I meet along the way.

  2. This is interesting. Does this mean that obesity can cause this new gene which in turn means that obesity can cause Alzheimer's disease. Interesting how this new gene affects leptin levels, which scientists are now finding that fructose in soft drinks, especially from high fructose corn syrup can affect and disrupt leptin. It will be interesting to watch further studies.

  3. Is there a free link to the full study or is it only for subscribers?

Sorry, the comment form is closed at this time.

Alz.org main site  |  Research  |  Advocacy  |  Care and support  |  Message boards  |  Disclaimer  |  Donate  |  Contact us  |  Sign up for e-news
© 2011 Alzheimer's Association | Blog Suffusion theme by Sayontan Sinha