Inherited gene changes take years off life expectancy

Researchers have linked a shorter lifespan with two common gene changes called variants. The researchers found these common variants near APOE and CHRNA3/5 genes to be associated with lifespan. One copy of either of these two changes to your DNA could shave a year off your life expectancy. People who inherit two copies, one from each parent of both variants could expect to lose about 3.3 to 3.7 years.

APOE gene has been linked to Alzheimer's dementia, high cholesterol, and coronary disease risk. The CHRNA3/5 gene is associated with an increased risk of lung cancer, nicotine dependence, and respiratory problems in smokers. Apparently These variants are pretty common in the population, as more than two-thirds of us will inherit a single copy of one of these DNA changes. And 3 in 1,000 people will inherit two copies of both variants. The variants have age and sex related effects on lifespan. The variant linked to Alzheimer's has a greater impact on older women, while the variation associated with lung disease influences middle-aged men more.



"Although the effect of these genetic variants on lifespan is surprisingly large, it is important to remember that this is only part of the story. Lifestyle has the greatest impact on how long we live and that is under our control." (Peter Joshi)

Original source: http://www.nature.com/ncomms/2016/160331/ncomms11174/full/ncomms11174.html
Related source: http://www.eurekalert.org/pub_releases/2016-03/uoe-igc033016.php

Gene Variants that could Shorten Lifespans

Researchers from the University of Edinburgh in the UK have identified two gene variants that can take up to 3 years off an individuals life. Working out everyday and eating healthy may not always guarantee a longer expected lifespan due to an individuals predetermined genome.The identified gene variants occur on genes referred to as APOE and CHRNA3/5. These gene variants are carried, at least independently, by more than 2/3 of the global population. However, only 3 out of every 1000 individuals carry both gene variants within their genomes.The presence of both these gene variants was seen in the genomes of individuals who died earlier than their calculated life expectancy.

 Although these genes have correlating effects, they are found on very separate parts of the individuals genome. 

The reasons why these genes have these effects are not yet clear, however, both genes have been linked to differing medical conditions known to shorten lifespans. CHRNA3/5 has been linked to a higher predisposition for lung cancer and severe respiratory problems. APOE has been linked with high risk of Alzheimer's disease, heart disease, and high cholesterol. All of these medical ailments alone can cause a lifespan to be shortened, so when combined the effects are more severe. The APOE variant effects more women then men, while CHRNA3/5 effects more men then women. However, when seen together these genes can effect the individuals life regardless of sex. Contrary to the appearance of this article how long you live is not solely dependent on your predetermined genetics. Lifestyle factors like environment also play a role in lifespan. The role of genetics in an individuals lifespan is very complicated, and much is still unknown. I am interested to see if the discovery of these gene variants leads to the discovery of other lifespan gene effectors. Or if more research on the determining factors of a lifetime are performed. 

Two common genetic variants connected to memory performance

            The researchers and scientists from Boston University School of Medicine “have discovered to common genetic variants that are believed to be associated with memory performance.” This is a giant step forward since it can help adults with dementia retain their memory for longer, and be independence for a bit longer. 

Alzheimers linked to Apolipoprotein E gene

The study was conducted under the data that was gathering through “Charge” which is an acronym for Cohorts for Heart and Aging Research in Genomic Epidemiology. They acquired their data from 30,000 dementia free adults over 45 years old, 11,000 candidates of European decent, along with approximately 1,500 young adults to have a comparison between the adults. They were examined by completing memory test that incorporated recalling memories, and they examine segments of their complete genome to certain points that they scored low on the test. In their studies they discovered that the Apolipoprotein E gene had a direct correlation to the candidates low score when remembering, and was known to be a risk of dementia. Along with a section of the genome involving the immune system also had a correlation to the candidates inability to remember.

This is great discovery since this will improve the understanding of memories, and will help people with Alzheimers retain their memories and remain a functional adult. This also shows that by a large collaboration of the scientific community pooling in their data will make it easier and increase the pace of research.  

Article:http://www.news-medical.net/news/20141125/Researchers-discover-two-common-genetic-variants-associated-with-memory-performance.aspx

2nd Article :http://www.myfoxal.com/story/27481703/researchers-uncover-clues-to-memory-performance-in-international-genetic-study

The Two-Faced Alzheimer’s Gene

         A team of researchers at Harvard University set out to understand gene apolipoprotein E or more commonly APOE and how it plays a role in Alzheimer’s disease. Currently this neurodegenerative disease is the 6^th leading cause of death in the United States. It is known that those carrying a specific version of the APOE called APOE4 increases the risk of developing late onset Alzheimer’s disease. The APOE gene is responsible for making proteins that transport cholesterol. Using mice with an “Alzheimer’s like disease” they injected each one with APOE2, APOE3 or APOE4. Mice that were injected with APOE4 had a 10% increase in plaque formation and amyloid beta. These plaque and amyloid beta tangles are a key suspected to play a key role in Alzheimer’s disease progression. Mice injected with APOE2 on the other hand were found to have a 10% decrease in these plaque formations and tangles. This research shows that while APOE4 decreases the number of synapse connections APOE2 protects them, mice injected with APOE3 were found to have no significant difference in Alzheimer’s symptoms. The findings of this study are exciting when thinking of the possibility of gene therapy. Currently about 14% of the population carries the APOE2 version of APOE while 7% of the population carries APOE4. The team now wants to look at ways to decreasing or inhibiting APOE2 and increase APOE2.
 

Link:

https://www.sciencenews.org/blog/scicurious/gene-boosts-alzheimer%E2%80%99s-risk-might-protect-against-it-too

Related Links:

http://www.medpagetoday.com/Neurology/AlzheimersDisease/43056

http://www.alz.org/

Gene that boosts Alzheimer’s risk might protect against it too

Different types of the APOE gene were put in mice in order to develop potential Alzheimer's disease treatments.  The APOE4 gene increased plaque formation and amyloid beta in the brains of mice; where as, the APOE2 helped to decrease plaque density and amyloid beta, which protected against Alzheimer's.  According to the study, an increase of APOE4 seemed to cause a decrease in synapses, while APOE2 appeared to protect neural connections.


In the future, treatments that in decrease APOE4 while increasing APOE2 may be developed to treat and/or prevent Alzheimer's.  Therapies or potentially drugs may be invented to manipulate the APOE gene.

Link to article

ApoE protein levels at older age may promote Alzheimer's disease

According to Science Daily, scientists at Gladstone institute found a further linkage between Alzheimer's disease and an ApoE protein. It is still unclear to the exact nature of how this protein works but it is found that at younger ages it helps to reduce the build up of amyloid-beta. This build up is found in most Alzheimer's patients, which scientists believe is a possible cause of this disease. The way ApoE works is at a young age the protein helps to clear away the amyloid-beta, but as age increases so does the protein level. With the higher level of protein amyloid-beta accumulated. It is believed that at a younger age there is less of this protein produced which allows it to work more efficiently. The findings suggest that by reducing the amount of protein produced at an older age it may still be able to lower amyloid-beta which then may combat Alzheimer's disease.

 

Testing for Alzheimer's Disease

            According to an article from Psych Central, researchers have developed genetic testing to inform individuals of their risk for developing diseases such as Alzheimer’s. Disease. Although the most controversial part of this genetic testing, is the question, of whether the test is sufficient enough to tell whether the disease is a definite determination if you will have the disease. The gene being tested, APOE, Apolipoprotein E, has been shown to significantly increase the risk of a person having Alzheimer’s although genetic inheritance is a major factor. The test raises concerns among the medical community, because there is no cure for Alzheimer’s, and the fact that an individual may or may not get the disease just based on the test alone, could be more harmful for individuals than beneficial.