It's been a while, but exciting things have been happening here at Compute Against Alzheimer's Disease (CAAD) headquarters. Using the preliminary data gathered from our initial analyses of the change in entorhinal cortex (EC) volume over time, we wrote a grant proposal for the National Institute on Aging (NIA)'s Small Business Innovation Research (SBIR) program. We were recently notified that our submission was accepted for funding to study the possibility of predicting Late-Onset Alzheimer's Disease (LOAD) endophenotypes!
While genotype data contains hundreds of thousands of... Read more
One of the benefits of the Compute Against Alzheimer's Disease campaign is the introduction of novel software to perform large-scale molecular dynamics simulations. The specific method used in this software is called replica exchange molecular dynamics (REMD). Usually, a high-powered computer cluster as can be found through Amazon or XSEDE is required to run REMD simulations. Our novel software alleviates this requirement and allows these simulations to be performed remotely, on personal computers scattered around the globe.
The difference in performance between REMD and conventional molecular dynamics (CMD) is... Read more
Hello! In this post, I'll give an update on some exciting results we have recently produced under the Compute Against Alzheimer's Disease (CAAD) project.
One of the first phenotypes we've chosen to examine is the change in the size of the entorhinal cortex (EC). The EC is one of the most significantly affected brain regions in Alzheimer's Disease (AD) patients. In fact, functional MRI (fMRI) studies have shown that the neural degeneration seen in AD... Read more
A hallmark of Alzheimer's disease is the accumulation of the amyloid β (Aβ) peptide in the brain. As Aβ accumulates, it aggregates into complex structures, forming oligomers (a collection of around 2-12 peptides) or long, insoluble fibrils. Only these aggregated forms are believed to have any cytotoxic effect responsible for Alzheimer's; the presence of a single Aβ peptide in the brain is likely innocuous.
The reason for this difference in effect of Aβ depending on its aggregation state is complicated. However, with new computing power and more sophisticated methods... Read more
Welcome! This is the first installation of the Compute Against Alzheimer's Disease blog. For this first post, I wanted to give you a bit of background on the work we're doing and why it's important.
Many previous genetic studies of Alzheimer's Disease (AD) have been stymied by the fact that diagnosis is very inconsistent, and the disease itself is very heterogeneous. This means that two patients who show the same symptoms may have very different underlying pathologies in their brains, while two people with similar pathologies may have very different outcomes. This can make it extremely difficult to... Read more