The genetic nature of Alzheimer’s disease is well established. If your parents or siblings suffered from the condition, you are considerably more likely to fall under its influence. A new study of brain protein variants has moved the scientific community closer to finding the underlying reason for this pattern and provided them with a new treatment target. The Translational Genomics Research Institute (TGen), a non-profit Arizona study group, already made news in 2006 by illuminating the importance of the KIBRA (kidney-and-brain) protein in human memory. Located primarily, as its name implies, in the kidney and the brain, KIBRA appears to play some sort of regulatory role in the cognitive process after being activated by the hippocampus, the area of the brain most active in the process of memory storage and recall.

Each gene consists of two opposing alleles, or markers, that help to define the individual in whom they’re found, and the combination of four allele varieties – A, C, G and T – accounts for both the amazing degree of diversity found within our race and the shared attributes of our family lines. In the earlier study, researchers at TGen found that one’s capacity for memory retention is determined by this particular gene. KIBRA, it turns out, helps to decide not only how well individuals can remember facts but also how susceptible they will be to the Alzheimer’s influence.

Using a variety of genome-mapping tools to examine the brain compositions of nearly 2,000 subjects both living and dead, researchers found that the KIBRA proteins in Alzheimer’s brains were considerably altered. They also found that individuals who lacked the protective “T” allele in their KIBRA genes did not perform as well on memory tests. Individuals 50 years and older who did not have the T variable also displayed less activity in the areas of the brain most prominently affected by Alzheimer’s. Their primary visual cortexes behaved normally, and this pattern mirrors the symptoms of Alzheimer’s. According to the two studies’ combined conclusions, individuals carrying the “C” variation of the KIBRA gene have inferior memories as they grow older; they also carry a greater risk of developing Alzheimer’s. KIBRA has not been linked to the development of Alzheimer’s quite as directly to as Apolipoprotein E, a molecule whose mutation leads to the degradation of other vital brain proteins. But the two factors appear to be intertwined. Researchers controlled for the Apolipoprotein E variable with no observed changes in their results. 

While the importance of this study may be difficult for the layman to discern, it could have considerable influence on the next generation of Alzheimer’s treatment methods. Early diagnosis has been established as perhaps the most important element of the treatment equation. The disease’s symptoms rarely show up until its presence in the brain is well-established and irreversible. If this research eventually leads to a greater number of effective early diagnoses, it could very well change the face of Alzheimer’s altogether.