neuroscience Archives - Sanford Burnham Prebys

Tag: neuroscience

Institute News

Scientists and artists unite in unique San Diego Art Institute exhibit

AuthorMonica May
Date

February 21, 2020

Neuroscientist LuLin Jiang and artist Becky Guttin pose next to Guttin’s installation, an allegory of Alzheimer’s in progress. Photo credit: Tim Hardy Photography.

What happens when scientists and artists connect? A powerful new exhibit at the San Diego Art Institute unites these seemingly separate worlds—attracting nearly 1,000 visitors to the show’s opening reception on Saturday, February 8.

Drawing from her lifelong love of science, curator Chi Essary paired 16 local artists with scientists from San Diego research institutions to create the show. LuLin Jiang, PhD, a neuroscientist at Sanford Burnham Prebys, was matched with Becky Guttin, an artist who specializes in sculpture, drawing, jewelry and more. 

“This project interested me because of the many parallels between art and research,” says Jiang. “As a scientist, I’ve always seen my role as bringing an invisible truth to light. I also welcomed the opportunity to help more people connect to science that one day may have a positive impact on their life.” 

The two met more than a year ago to discuss Jiang’s research into the underlying cause of Alzheimer’s disease. They had their work cut out for them: Jiang’s research takes her deep into the unseen realm of brain cells and molecules. 

Guttin described the inspiration behind her piece. 

“I read and reread my notes. I remembered hearing the words ‘dirt,’ ‘clean’ and ‘dust’ repeated, referring to beta amyloid accumulating in the brain,” says Guttin. “I realized that instead of buying new materials, I needed something that was not new but had dirty residues from past lives.” 

Guttin focused on recycled plates from printing shops—their ink still visible. She contrasted the gray plates with fresh green grass and a branching, neuron-like tree, creating a stunning installation that is an allegory of Alzheimer’s in progress. Symbols of life, growth and degeneration are represented throughout.

The piece spoke to many individuals who attended the opening-night reception. 

“Many people told me their personal stories about losing loved ones to Alzheimer’s disease and wondered if we will ever find a cure,” says Jiang. “This experience left me even more motivated to continue my research to find treatments for Alzheimer’s disease.” 

The installation is on display in the Illumination exhibit until May 3, 2020. The show is free and open to the public.

Institute News

Attacking Alzheimer’s disease by controlling toxic proteins

AuthorBill Stallcup, PhD
Date

August 25, 2017

Alzheimer's disease - neurons with amyloid plaques shutterstock_111506315

The formation of amyloid-b plaques (aggregates of the amyloid-b protein) in the brain is one of the hallmarks of Alzheimer’s disease, a pathological disorder in which the death of neurons leads to dementia. Although the details involved in this process are still highly debated, many researchers agree that excessive levels of amyloid b protein (Ab for short) lie at the root of the disease. Accordingly, much research is currently focused on determining the cause of Ab build-up.

Huaxi Xu, PhD, professor and Jeanne & Gary Herberger Leadership Chair in Neuroscience at SBP, explains that, “Ab is a fragment derived from a larger protein called amyloid precursor protein (APP). The toxic Ab fragment is produced by the action of enzymes that operate inside the cell. In contrast, the action of enzymes that operate outside the cell produce a different set of non-toxic fragments of APP that are part of a normal APP recycling/replenishment system on the neuron cell surface. We wondered if we could minimize the toxic cleavage events that occur inside the cell by promoting the non-pathological, cell surface recycling of APP.”

In a recent report in the Journal of Neuroscience, the flagship journal of Society for Neuroscience, the Xu lab identified candidate molecules that might be important for promoting the cell surface recycling of APP. According to post-doctoral associate Timothy Huang, PhD, first author on the paper, “Loss of a recycling protein called SORLA has been observed in Alzheimer’s patients. Our experiments show that SORLA forms a complex with an intracellular navigational protein, SNX27, which can redirect SORLA and its binding target APP to the cell surface. On the surface, APP mostly undergoes non-pathological processing rather than generating Ab.”

Further validation of this inside versus outside concept was achieved by tweaking cellular levels of SORLA and SNX27 in cultured neurons. Increasing the levels of SORLA and SNX27 resulted in higher levels of APP on the cell surface, thus avoiding production of the toxic Ab fragment. In contrast, decreasing the levels of SORLA and SNX27 kept APP largely inside the cell, thus increasing its vulnerability to pathological cleavage.

Xu emphasizes that future work will need to aim at determining whether these SORLA-SNX27-APP interactions can be exploited in mouse models of Alzheimer’s as a means of preventing or lessening the effects of the disease.