Mapping a Monkey Brain May Aid Gene-Driven Alzheimer’s Prediction
Recently, the Proceedings of the National Academy of Science (PNAS) published an article describing the successful completion of IBM researchers mapping neural pathways of a macaque monkey. IBM’s interest? One of IBM’s chief interests is looking at design in substrates that can generate lots of intelligence in small spaces. Being smart about squeezing lots of intelligence in physically small spaces can be used when designed next generation computer chips. Indeed, one of the findings IBM was interested in is how architecting intelligence in a space-limited network (like the brain, which is bounded by the skull on the upper plane and by quantum physics at the lower plan) is different from the unlimited space of a social network.
The PNAS article included this comment (emphasis ours)
“We derive a unique network incorporating 410 anatomical tracing studies of the macaque brain from the Collation of Connectivity data on the Macaque brain (CoCoMac) neuroinformatic database. Our network consists of 383 hierarchically organized regions spanning cortex, thalamus, and basal ganglia; models the presence of 6,602 directed long-distance connections; is three times larger than any previously derived brain network; and contains subnetworks corresponding to classic corticocortical, corticosubcortical, and subcortico-subcortical fiber systems.”
Why is deeper analysis of brain networks important for the genetic predictions of Alzheimers? Genetic testing for Alzheimer’s risk is at a standstill of sorts. Consider this snippet from a widely read article on the limitations of genetic screening testing for Alzheimers:
“For the majority of people who are at risk for the late-onset form of Alzheimer’s disease, the most important factors are age, female gender, family history, and presence of the gene APOE4 . Even though people who have the APOE4 gene are more likely to develop Alzheimer’s, genetic testing is not very useful because so many people who have APOE4 don’t go on to develop Alzheimer’s, and there are plenty of people who don’t have APOE4 that do develop Alzheimer’s.”
It seems likely that APOE4 alone is not a good indicator. What will be a much better indicator are multiple markers. One approach for finding multiple markers is looking for single markers like APOE4; a better approach is to look down neural pathways to find where APOE4 is acting together with other genes—and their joint activity, decay, presence, or absence is a much higher correlate. This is impossible without much deeper understanding of where the brain rural routes, highways, freeways, and superhighways exist.