At the beginning of the discussion, she gave me the DVD, "Can Alzheimer's be stopped?"
These DVDs were sitting around for some reason. My guess is, they were distributed in the department as an educational aid. She's had at least three copies in the office.
So tonight I popped the DVD in my laptop and watched. 60 minutes, plus short (<5min) bonus films.
The 2016 Nova/PBS documentary was very well made. It can be quite engaging, too.
This documentary was made for general public. It was a good description of ongoing battle (or perhaps, struggle) by research industry and patients against the disease.
When we read research papers and reviews, they are great sources of knowledge. At the same time, they are highly condensed, in terms of information.
What was presented in the documentary was something I knew already, mostly by reading, and some by experience. Yet, with all real life settings and with human voices and faces, the knowledge was given so much more "reality".
There are many layers in knowledge, depending on your standpoint.
[Producer] I am doing research on Alzheimer's now. That is a hands-on researcher's standpoint. Since the mouse model we uncovered and are working on is a novel model, what we are doing is cutting edge scientific research. We are on the side of producing latest knowledge on the disease.
[Consumer] Then there are written knowledge from colleagues. We read through results of their 3+ years study in 15 minutes, and see if they can be useful for our own study.
[Teacher] The colleague is busy teaching in the department. I borrowed her course slides for neurodegenerative diseases (including Alzheimer), just to know how the subject is taught in college in 2018. Teaching requires different way of objectifying the body of knowledge and assessing students' existing knowledge.
[Patients' family] I would not be working on Alzheimer's, if my mother was not diagnosed as Alzheimer's in 2015. Her diagnosis motivated me to read and learn about the disease. Since she lives in Japan, the disease impact is not direct. Yet, I've seen how the disease goes, and it is tough to see or hear at times.
Being a researcher is unique privilege, I'd say. In the process of reading literature on Alzheimer's, I learned that what I study ("genomic instability in the body" research theme) may be involved in causing or aggravating Alzheimer's disease. Since I've been working with genomic instability mouse models, I tested the hypothesis with the genomic instability models that were intentionally maintained and aged for cancer study purpose at the time.
Although with a twist (research is not always straightforward), the test led to our finding of the model mouse that accumulates amyloid-beta in the brain in old age.
Previously, it was believed that normal mice will not develop amyloid-beta in the brain, due to sequence difference in mouse version of amyloid precursor protein and to their shorter lifespan (2-3 years) compared with human (65+ years for 95% of Alzheimer's). It was believed that to generate amyloid plaques in mouse, manipulation of amyloid metabolism and forcible expression are needed.
Our mouse is designed to create "cohesinopathy", a type of genomic instability that naturally occurs over age, which also is associated with human Alzheimer's disease. With a transgenic mutation, the model spontaneously accumulates amyloid-beta, the initial trigger and a pathological cause for Alzheimer's disease, in old age.
We are getting flurry of data that show similarities between the mouse's brain and human brains with Alzheimer's disease. We are very excited by that.
What we do is work in the lab, called pre-clinical translational study. Yet, for uncovering disease mechanisms and biomarkers, the mouse will be immensely useful. The knowledge we know is not yet directly translated to human patients. Hopefully it will, soon.
Sure, if our study turns out to be successful and helps to cure human Alzheimer's disease, Nova/PBS may be making a documentary out of our work. Haha.
