The Taube Koret Center Blog

The robotic Microscope allows researchers to graduate from population studies to longitudinal studies of individual neurons.

Huntington’s disease (HD) is a debilitating fatal disease caused by a mutant gene that that has a repeating sequence. In general, the more repeats, the earlier the onset of the disease is. However, the length of the repeated sequence accounts for only part of the variability of the age of onset. Could other factors be involved? Dr. Julia Kaye and her team at the Taube-Koret Center use a technique called whole-genome sequencing to try to find pieces of DNA called genetic modifiers that are involved in coding as well as non-coding proteins that might modify the age of onset. They hope to identify new genetic modifiers to help them understand the factors that determine age of onset in HD and shape the search for HD therapies down the road.

My path to becoming a scientist was non-traditional. I grew up in Canada and due to a turbulent family situation left home and school at the age of 15. Returning 12 years later I started classes at Foothill College and discovered a passion for science. I got involved with research immediately upon transferring to UC Berkeley and as an undergraduate and master’s student at UCB, I studied environmental endocrinology with Dr. Tyrone Hayes, performing field studies in Africa and the American Midwest. My research with Dr.

Neurons are the structural and functional blocks that make up the human nervous system. Neurodegenerative disease is a broad terminology that encompasses various conditions resulting in the progressive death of neurons, such as Parkinson’s disease (PD), amyotrophic lateral sclerosis (ALS), Huntington’s disease (HD), and Alzheimer’s disease.

Sadly, no disease-modifying therapies are available for any of these diseases. There are several reasons for this lack of treatments.

Lack of disease models that faithfully replicate disease characteristics:

Take a quick scan around you, and what do you see?

Everything we see is, in fact, composed of elementary particles of light called photons that reflect off of the objects in our visual path. Our eyes collect these reflected particles and, with the help of our brain, generate images for us to see. Although the human eye consists of remarkable machinery that enables us to interact with the world, it has some limitations.

First, our eyes have evolved to capture only a fraction of the light emitted by the sun, which we refer to as “visible” light.

Having grown up in a coastal town, the smell of the ocean evokes strong memories. Images of days in the sun, sounds of the crashing waves, the feeling of sand between my toes, the taste of salt water, and the joy of a relaxing afternoon replay in my mind’s eye like a faded home movie of experiences long since passed. The power of memory allows us to create and access a mental representation of the world, or to be swept up in the emotions of previous events. What is this ability to store and access information?

Jeannette Osterloh was a postdoctoral fellow in Steve Finkbeiner’s lab at the Gladstone Institute for Neurological Disease from 2013-2017. She attended California Polytechnic State University for her undergraduate education and the University of Massachusetts Medical School for her graduate studies. Her research focuses on modeling human neurodegenerative diseases in induced pluripotent stem cells (iPSCs). She specifically focuses on amyotrophic lateral sclerosis (ALS) and is “trying to figure out what goes wrong at a cellular level in early stages of the disease, with the goal of identifying therapeutics” (Jeannette). Cultivating these types of cells can be very labor intensive, and Jeannette can be found in our tissue culture room almost every day.

The human nervous system is incredibly complex. With careful experimental design, we generate simpler models of the brain in the laboratory. Models come in many forms, including using cancer cell lines, primary cells (taken directly from an animal and grown in a dish), and whole animal models.  Every model has its strengths and weaknesses, but so far, no model has produced effective drug treatments for most neurodegenerative diseases. Because of this, we have turned to an emerging and exciting new model system that uses human stem cells.

The Taube Koret Center was established in 2009 with gifts from Tad Taube Philanthropies and the Koret Foundation and with Dr. Steven Finkbeiner as Director. The mission of the center from its inception is to find therapies to treat devastating neurological diseases such as Huntington’s disease, amyotrophic lateral sclerosis, frontotemporal dementia, Parkinson’s disease, and Alzheimer’s disease.


The Taube-Koret Center aims to accelerate the discovery of therapies for neurodegenerative diseases including Alzheimer's, Parkinson's, Huntington's and amyotrophic lateral sclerosis. Venture philanthropy support from Mr. Tad Taube (Taube Philanthropies), Mr. Jeff Farber (Koret Foundation), and Mr. Warren Hellman (Hellman Family Foundation) established the Center. Industry drugdiscovery experts work with academic researchers to design and execute performance-driven programs to develop discoveries until they fail a milestone or until they are partnered.