I want to convey our deep appreciation to everyone for supporting our research on Alzheimer's disease! Thanks to you, we have reached our fundraising goal of $15k. This will allow us to fund stipends for undergraduate students to fight Alzheimer's disease rather than work extra at part time jobs. Your generous contributions will also support our grad students to train them.

When I teach my upper level Neurogenetics course here at UT Austin, most undergrads are only interested in neurological conditions that affect their peers. This includes drug and alcohol addiction, bipolar disorder, and schizophrenia. Despite being the 6th leading cause of death, and the only disease in the top ten causes of death with no effective medicine, Alzheimer's disease is not usually on the minds of your typical college student. Alzheimer's disease mainly affects the elderly which seems like a long way off to college students. By introducing UT college students to Alzheimer's disease research, and by opening the door to academic classes where they can befriend adults with Down syndrome who are all predisposed to Alzheimer's disease, college students wake up to the seriousness of this terrible disorder. After this experience, most students on medical and research tracks adopt the mission of fighting Alzheimer's disease even after they graduate. By training this bright young group of future leaders, you are helping to defeat Alzheimer's disease.  

Although we have reached our original fundraising goal, we have one more day to raise funds via Hornraiser. So I am asking us to jump a little higher to reach a "stretch goal" of $18k total to fund an innovative experiment. This extra $3k in funds would allow our lab to purchase time throughout the summer to use a special automated scanning machine. With this automated device, we can scan the glowing neurons of worms like a laser at the supermarket. By culturing worms in thousands of different conditions in tiny plastic wells, we can determine which drugs and environmental conditions enhance or prevent neurodegeneration.  If drugs or conditions stop the neurons from dying, the machine will note the bright glow from healthy neurons in our Alzheimer's worms. Please consider sharing this goal with your friends and family who care about defeating Alzheimer's disease.

Thank you for your continued support!!

Thanks again to so many of you who have donated and spread the word regarding our fundraising campaign to support funded research opportunities to undergraduates in Alzheimer's disease research!! So far we have made it more than half way towards our goal with just over one week left. Please help us in this last stretch to reach our full goal by spreading word to your friends and family who care about defeating Alzheimer's disease.

I feel passionate about training undergraduates.  I'm very proud that we have taken excellent students at UT Austin and launched them into the most prestigious research programs in the country. Below are shining examples of some of our recent student volunteers.

Celia Beron

Celia joined our lab after Freshman year not knowing much about research. She quickly picked up skills in a project that allowed her to win summer research fellowships at Univ Washington and the prestigious Janelia Farm research center. By the end of her time in our lab she had contributed to a project highlighted on NPR radio, and moved on to publish her own first-author paper on novel way to potentially treat muscular dystrophy. Her amazing dedication and intellect was recognized by all graduate programs that accepted her. Celia settled for the graduate program in neuroscience at Harvard University.

Lindsay Becker

Lindsay started in our lab working on a complicated project involving molecular basis for how alcohol alters the nervous system for intoxication. She then completed an independent project on how dopamine is used in switching the nervous system from one mode of motion to another. Lindsay now is almost finished in the graduate program in neuroscience at Stanford University where she has been studying the basis for ALS. In addition to the papers she published while volunteering in our lab, she recently had her ALS research accepted into the most competitive journal in the world called Nature. 

Erin Elbel

Erin joined our lab thinking that she'd like to aim for a medical career after graduating UT. She focused on studying genes that underlie disinhibition during intoxication, helping our grad students publish a well received paper. She used her experience in our lab to jump into medical school at Columbia University where she still loves studying neurology.

Lindsay Brettmann

Lindsay represents another student who loved research and took this into a medical direction. During her time in our lab, she screened for novel mutations that "cured" a worm model of Parkinson disease. Without any dopamine, these magical mutations allowed the worms to move about like normal worms. Lindsay soared with success, first with an extremely competitive Fulbright Award to study Spanish in Spain and next entering medical school at UTSW in Dallas.

All of our undergraduate students experience real research firsthand. Students who work on our Alzheimer's research will be more likely to continue groundbreaking Alzheimer's research in competitive grad and medical school programs. By supporting this fundraiser you will both make a difference with discoveries in our lab at UT Austin while launching the careers of these bright young researchers!! Thank you for your support!

Thank everyone for your strong support!! We are very grateful for donations large and small to support this life-changing opportunity to train undergraduates in Alzheimer’s disease research in our lab. Please continue to spread the word to your friends and loved ones via email and social media about supporting this important cause!

I want to share a special thanks to the Down Syndrome Association of Central Texas (DSACT)!!! This organization supports educational and recreational activities for people with Down syndrome and their families. They also do justice by advocating public policies that make life easier and fair for people with Down syndrome. Most impressive, not complacent with helping people with Down syndrome in the present, they also invest in a brighter future for people with Down syndrome by supporting groundbreaking research on Down syndrome and Alzheimer’s disease at both local and national levels. Our UT students thank DSACT for their generous and empowering donation towards our mission. Please check out the DSACT website to see their range of activities and projects supporting people with Down syndrome! They still have tickets available for their Cocktail Bash on April 12, 2017.

Photo of my son, Ocean Pierce-Shimomura, enjoying a giant lightbright at the Thinkery  Museum in Austin, TX.

Most Alzheimer's research uses mouse models. This is because mice show a decline in memory as they age when engineered with human Alzheimer's disease genes. They even show a buildup of toxic peptides derived from the APP molecule, including plaques, in brain regions associated with memory. Researchers have used mice to develop a number of drugs currently in clinical trial such as ones targeting toxic peptides derived from the APP molecule.

Although powerful, unfortunately mouse models of Alzheimer's disease have two main disadvantages. First, most mouse models do not display neurodegeneration. This has forced many researches to study how drug and genetic treatments alleviate plaques in mice rather than study how these treatments may stop neurons from dying. This has become an important issue as researchers debate whether the plaques are harmful or harmless in Alzheimer's disease. Second, it takes many months to two years for mice to show signs of cognitive dysfunction or plaque buildup. Although this sounds a lot faster than the typical 75 years that it takes for most people to develop Alzheimer's disease, it significantly slows down the number of experiments that can be tested and raises cost to house and care for these precious mice.

To surmount these two major problems in mice, we engineered a tiny worm to carry human Alzheimer's disease genes. When we make them carry human APP, we find that a small number of their neurons die when they reach middle age adulthood. Because worms age fast, neurons die within only one week!  You can even see the neurons that we engineer to glow green through their transparent body in the photo below. Recently, when our graduate student Momo Sae-Lee added the APOE4 gene, we discovered that this hastened the death of the same neurons, while also killing a second subset of neurons. APOE4 by itself had no such effect. This mysterious synergy between APP and APOE4 has also been observed in Alzheimer's patients. It is very easy to tell if these neurons die, because it interferes with their ability to move. All we need to do to determine if the neurons are dead or alive now is to count the number of moving worms.

With our new ultrarapid model of Alzheimer's disease, our lab is poised to train undergraduate students to test what combination of drugs and genetic manipulations prevent neurodegeneration. With the speed afforded by this worm model, we can ask: How do drugs currently being tested in Alzheimer's disease patients work? What target do they bind to in the nervous system? How does this mitigate neurodegeneration?  We can ask these questions in the simple worm because its genome is considerably complex -- they share almost all of the same genes as humans.

Please consider supporting our Alzheimer's disease research and undergraduate training and spreading word about this promising research to your friends. Thank you!!

Thanks to several early donors for kick starting our fundraising campaign!

I wanted to share with you a personal story. Our research on how the plaque protein APP and unlucky APOE4 gene increases risk of Alzheimer's disease is not only scientific but also a personal mission.

I became interested in finding treatments for Alzheimer's disease once my son (pictured) was born with Down syndrome in 2001. You probably didn't know this, but virtually all adults with Down syndrome develop early onset Alzheimer's disease. This is because they carry an extra 21st chromosome which harbors a gene for the plaque protein gene APP. One extra copy of the APP gene is all it takes to develop Alzheimer's between the ages of 40-60.  This connection between Alzheimer's and Down syndrome is what led researchers in the 1980s to narrow down the discovery of the APP gene.

My personal connection to Alzheimer's grew stronger three years ago. Then, I was teaching my upper level neurogenetics class where I allow students to learn about genetics by browsing my genome. Together we learned that I may carry two copies of the unlucky APOE4 gene. I knew that this would predispose me to late onset Alzheimer's disease. Overall, the unlucky pair of APOE4 genes leads to a 91% chance of developing Alzheimer's disease in my life, and usually by the age of 68. Sadly, with my gene my son with Down syndrome will likely develop his Alzheimer's faster and more aggressively. Coincidentally, my parents contacted me concerned that my mother (pictured) was having problems with memory. She was 68 year old at the time. The coincidence almost guarantees that she also carried the unlucky APOE4 genes too.

So now compassion for my mother and son is making me laser-focused on conducting innovative research to benefit people suffering from and predestined to Alzheimer's disease. Please consider contributing what you can to help us fight Alzheimer's disease through our research and training of undergraduates. You can also make a huge difference simply by spreading word about our campaign to your friends and relatives who care about Alzheimer's disease by email or social media.

Thank you!  - Jon Pierce, Associate Professor, UT Austin