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We know that Alzheimer's is a complex disease encompassing an interactive cascade of pathological processes. Understanding those processes, the mechanisms that trigger them, and beneficial ways to intervene against them, are all topics of intense scientific scrutiny.
This week, that scrutiny uncovered another piece of the puzzle and created a new challenge to understand where and how it fits into the bigger picture.
Research conducted at the University of Miami, and published in PLoS Genetics, showed that variations in the MTHFD1L gene were highly correlated with Alzheimer's disease. In fact, those with a specific variation were about twice as likely to develop Alzheimer's disease as those without it.
This gene also plays a role in regulating the body's level of homocysteine, an amino acid affecting cell metabolism. This discovery seems integral in understanding Alzheimer's because, aside from the high correlation between the genetic variant and the presence of disease noted in this study, high levels of homocysteine were already known to be a risk factor for the Alzheimer's.
As suggested by the headline of this post, this scientific advance provided no new answers; it only uncovered another piece of the puzzle that must be fit into the complete picture before we can fully understand how best to intervene against Alzheimer's. Nonetheless, it is exciting because we cannot hope to fit the puzzle together until all the pieces are in hand, and this is another small but important step toward that end.
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A better understanding and more awareness of Alzheimer's related issues can impact personal health decisions and generate significant impact across a population of aging individuals. Please use the share buttons below to spread this educational message as widely as possible.
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