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Family history of Alzheimer’s, length of gene impacts risk for disease: Study

Washington: A study finds that late middle-aged people, with a family history and longer version of mitochondrial gene, encountered twice as much memory loss up to 10 years later as someone with a family history and a short version of the gene.

It is the most common form of dementia, characterised by progressive neurodegeneration that results in memory loss.

The study also found an association between the gene, family history and mitochondrial function, which creates energy to power cells.

Lead study author Auriel Willette said that the researcher who initially discovered the gene, TOMM40 (Translocase of Outer Mitochondrial Membrane-40kD), found it increased the risk for

Alzheimer’s.

The paper published online in journal of Alzheimer’s & Dementia.

“It was kind of a shot in the dark, but we found if you don’t have a family history of Alzheimer’s disease, then having a longer version of the gene is a good thing. It is related to better memory up to 10 years later and about one-fifth of the risk for developing Alzheimer’s

disease,” said Willette.

The team tracked changes in memory loss and cognitive function over time for middle-aged people at risk for Alzheimer’s, while the other group tracks similar changes in older people with and without the disease.

However, if your mom or dad has Alzheimer’s, then having a long version is bad. It’s a complete polar opposite.

The findings indicated that late middle-aged people with a family history and longer version of the gene encountered twice as much memory loss up to 10 years later as someone with a family history and a short version of the gene.

A similar but stronger finding was seen in a separate group of older adults with and without Alzheimer’s.

This study is an effort to lower the risk for Alzheimer’s, and ultimately prevent people from getting the disease.

The overall direction of their work focuses on how the body derives and processes energy, he said.

While this study examines mitochondria, the team also looked at insulin resistance and proteins and enzymes that cause problems regulating energy.

Willette stated that collectively, researchers are learning what happens to memory and cognitive function when brain cells do not get enough energy to do their job, causing long-term damage.

With all these different factors, the challenge is pinpointing why some people get Alzheimer’s and others do not. (ANI)