Julie K. Andersen, PhD, Professor

On the road to novel therapeutics for Parkinson’s and Alzheimer’s disease

As a renowned expert on age-related neurodegenerative disease, Dr. Andersen is pursuing a wide array of leads toward treatments for complex disorders including Alzheimer’s and Parkinson’s disease. Recently, the laboratory has joined efforts with the Lithgow laboratory at the Buck institute as part of a collaborative project aimed at identifying novel drugs that eliminate neurotoxic protein deposits in patients diagnosed with these devastating disorders. This would fill critical unmet need for drugs that can block disease progression in the brains of patients already impacted by these conditions.  

Lysosomes are organelles that serve as the garbage disposal of the cell. Damaged proteins and other cellular components are broken down by lysosomes in a process known as autophagy. Autophagy has recently been found to be a crucial factor in the removal of damaged neurotoxic proteins associated with several age-related neurodegenerative diseases including Alzheimer’s and Parkinson’s. Joint research from the Andersen-Lithgow laboratory has recently identified a factor called TFEB as being critical to this process.  A recent drug screen performed by our laboratories has identified a novel series of potent, structurally-related compounds that activate TFEB and prevent neurodegenerative phenotypes in C. elegans models of Alzheimer’s and Parkinson’s disease. Independent bioinformatic analysis suggests that these compounds have favorable characteristics for CNS-acting drugs in humans including high brain availability and low toxicity. We propose that these drugs have the wide-ranging potential to impact on all patients diagnosed with age-related neurodegenerative disease. Current efforts are towards pre-clinical studies in order to provide appropriate proof-of-principle to move forward into human phase I trials. A recent independent study from the Andersen laboratory has also identified lysosomal dysfunction as a prime driver of elevated toxic iron levels which occur in these disorders and suggests that thes drugs may provide additional benefit by preventing associated brain metal toxicity.

In a recent collaborative effort with the Campisi lab, the Andersen lab has shown that a process known as cellular senescence, previously associated primarily with aging in peripheral tissues, may also play an important role in age-related brain pathologies. The laboratory is working to identify novel 'senolytics', compounds which preent age-related brain senescence, as a novel potential cure.   

The Andersen lab is also involved in identifying potential biomarkers for Parkinson’s that may allow early interventional therapy.

Dr. Andersen was born in Great Falls, Montana. She earned a doctorate in Neuromolecular Biology at the University of California, Los Angeles (UCLA). She completed a postdoctoral fellowship at Harvard Medical School and Massachusetts General Hospital before going to the University of Southern California as an assistant then an associate professor at the Andrus Gerontology Center. She joined the Buck Institute in 2000.

Media Expertise
Dr. Andersen welcomes media inquiries on the following subjects:
Parkinson’s disease, risk factors: genetic and environmental; therapeutics.

Phone: 415-209-2070

Administrative Lab Coordinator: Mary Redwine
Phone: 415-209-2237

“My greatest hope is that our work here at the Buck will allow us to diagnose neurodegenerative diseases at the earliest possible stage, so treatment can begin before these conditions have a chance to progress.   That would free patients to live fulfilling lives without major disability.’’ 

- Julie K. Andersen, PhD


Recent Publications


Shankar J Chinta, Georgia Woods... Julie K Andersen "Cellular Senescence Is Induced by the Environmental Neurotoxin Paraquat and Contributes to Neuropathology Linked to Parkinson's Disease." Cell Rep 22:4 930-940
Anand Rane, Subramanian Rajagopalan... Julie K Andersen "Hsp90 Co-chaperone p23 Contributes to Dopaminergic Mitochondrial Stress via Stabilization of PHD2: Implications for Parkinson's disease." Neurotoxicology 65 166-173
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