Andersen Lab

Julie Andersen, PhD

Professor

On the road to new therapeutics for neurodegeneration, including Alzheimer’s and Parkinson’s disease.

Lab focus

The Andersen lab concentrates on understanding the underlying age-related processes driving neurodegenerative diseases in order to identify novel therapeutics that slow or prevent them from occurring. These include small molecules that boost the cell’s own ability to remove damaged proteins and other cellular components through a process called autophagy or those capable of removing cells which can inflict damage on healthy neighbors via a process called cellular senescence. We collaborate with other Buck researchers in order to understand the mechanisms involved and to screen and test novel compounds in various preclinical models of disease, including human induced pluripotent stem cells (iPSCs), C. elegans, and mice.

Why it matters

The most predominant neurodegenerative disorders currently afflicting the world population are Alzheimer’s disease and Parkinson’s disease. Most studies to date have concentrated on how these diseases differ. This “isolationist” approach has yielded few, if any, effective treatments for either disease. Aging is the major risk factor for both. The aging process itself is associated with cellular changes in the brain that likely drive functional deficits in cognition and motor movement. We believe that focusing on what these disorders have in common — the aging brain — will open up novel avenues for disease prevention, amelioration, and cures.

The Buck’s focus on aging as the common risk factor for chronic disease – including neurodegenerative diseases – takes research out of ‘silos’ and increases the odds of developing new therapeutics for these devastating conditions.

Julie Andersen, PhD

The Andersen lab is pleased to acknowledge the generous support of the following major funders:

Dr. Andersen received her PhD from the Department of Biological Chemistry in the David Geffen School of Medicine at the University of California, Los Angeles. She received additional research training in the Department of Neurogenetics at Massachusetts General Hospital in Boston. Prior to arriving at the Buck Institute, Dr. Andersen held a faculty position in the School of Gerontology at the University of Southern California.

Dr. Andersen has published more than 170 scientific papers and holds three current patents. She has been recognized for her research with a Parkinson’s Pioneer Award from the National Parkinson’s Foundation, a Glenn Award for Research in Biological Mechanisms of Aging, and a senior scholarship from the Ellison Medical Foundation. She was elected a fellow of the Society for Free Radicals in Biology and Medicine in 2013. She currently serves on the scientific advisory board for the University of Pittsburgh Medical Center’s Biology of Aging Program, on the editorial board of e-Neuro (Journal of Neuroscience’s e-journal), as a member of the Brookdale Institute on Aging, and as a council member for the Society of Neurotoxicity. Dr. Andersen has extensive experience working with both biotech companies and medical foundations, including Roche, the Michael J. Fox Foundation, the National Parkinson’s Disease Foundation, and the American Parkinson’s Disease Foundation.

  • Josue Ballesteros, PhD  Postdoctoral Research Fellow

    Josue received his bachelor’s degree in biochemistry from the University of Salamanca, Spain, in 2012. He then worked as a research intern at the Department of Experimental Pathology at the University of Bologna, Italy, where he studied mitochondrial DNA rearrangements during aging. He continued his education at the University of Iceland where he completed his PhD in 2019, investigating the interplay between the MiT-TFE transcription factors in melanoma and their role in autophagy modulation.

    JBallesteros@buckinstitute.org

  • Manish Chamoli, PhD  Research Scientist, Larry L. Hillblom Fellow

    Manish obtained his five-year integrated master’s degree in biotechnology in 2009 and then joined the PhD program in aging biology at the National Institute of Immunology in India. His PhD work was focused on understanding molecular pathways mediating dietary restriction–induced longevity using the C. elegans model. His research was supported by a fellowship from the government of India’s Department of Biotechnology. After completing his PhD in 2015, Manish joined the Lithgow lab as a postdoctoral fellow. Currently he is working in collaboration with the Andersen lab to understand the role of autophagy in aging and age-related neurodegeneration, utilizing novel pharmacological agents. He is supported by a three-year postdoctoral fellowship from the Larry L. Hillblom Foundation.

    MChamoli@buckinstitute.org

  • Suckwon Lee  Research Associate

    Suckwon Lee was born and raised in Seoul, Korea. Suckwon attended University of California, Davis where he got his degree of bachelor of science in biochemistry & molecular biology and departmental citation. After graduating from Davis, he wanted to broaden his skill set. His graduation from Cornell University in Masters of chemistry & chemical biology has made him equip chemical techniques more deeply than before. Following his all studies, he plans to use all the techniques and knowledge for his own unique research, related to aging.

    SLee@buckinstitute.org

  • Jenny Hong Yu Ng  SENS Post-Baccalaureate

    Jenny is a research scholar who joined the Andersen Lab in September, 2021 as part of the SENS Research Foundation post-baccalaureate program. She attended Cornell University where she received her bachelor's degree in biologicalsSciences. Her undergraduate thesis investigated the inflammatory and recovery profile in Acomys cahirinus (spiny mouse), a novel model known to be capable of epimorphic regeneration, upon sciatic nerve injury. Currently she focuses on the gut-brain axis and its immunological implications in Alzheimer’s.

    JNg@buckinstitute.org

  • Anand Rane  Lab Manager & Research Associate II

    Anand is from Mumbai, India, and received a master’s degree in biomedical sciences from Louisiana Tech University. He has been involved in basic scientific research in the Andersen lab over the past 12 years and has been working to understand the neuropathology underlying Parkinson’s disease to uncover both novel treatments and cures for the disorder. He is the co-author of 22 publications. Anand’s most recent independent research project involved identifying inhibition of the heat shock protein co-chaperone p23 as a novel therapeutic target for Parkinson’s disease.

    ARane@buckinstitute.org

  • Minna Schmidt  Postdoctoral Research Fellow

    Minna graduated from Lowell High School in San Francisco as an AP honors student in chemistry and physics. After completing a year at City College of San Francisco, she attended Brandeis University, where she received a bachelor’s degree with honors in chemical biology in 2013. She subsequently completed her master’s degree in chemistry at the University of California, Santa Cruz, in 2015, as well as received her PhD from the joint Buck-USC Biology of Aging program in 2021. Minna has pursued the characterization of novel small chemical compounds that act to prevent neuronal cell loss associated with Parkinson’s disease (PD.) She has a particular emphasis on inducers of hypoxia inducible factor 1 alpha (HIF1alpha), which previous publications from the Andersen lab have suggested serve a neuroprotective role in the disease. Minna’s current focus involves the study of exercise mechanisms in effecting changes to alpha-synuclein protein aggregation, a neuropathological hallmark of PD, by utilizing cell culture and C. elegans worm models.

    MSchmidt@buckinstitute.org

  • Chaska Walton, PhD  Research Scientist

    Chaska received his bachelor’s degree in psychology from the University of Barcelona, Spain, in 2013. He then did a Master in Neuroscience while working as a research intern at the department of Psychobiology at the University of Barcelona, where he studied cognitive enhancement by glutamatergic receptor modulator compounds in rat models of aging. He continued his education at the CSIC/Autonomous University of Madrid, Spain, where he completed his PhD in molecular bioscience in 2018, investigating neuronal cell division in mouse long-term primary neurons.

    CWalton@buckinstitute.org

  • Georgia Woods, PhD  Staff Scientist

    Dr. Woods received her PhD in neuroscience from University of California, Davis, where she used advanced microscopic techniques to study synaptic pruning in the developing rodent brain. She joined the Buck Institute in 2013. Georgia’s expertise in neurodevelopment and microscopy have laid the foundation for conducting translational research in the Andersen lab, illuminating cellular pathology in neurodegenerative diseases. In particular, her interests lie in elucidating how glial cell dysfunction in the aging brain contributes to all-too-common neurodegenerative diseases in aging populations, including Parkinson’s and Alzheimer’s diseases.

    GWoods@buckinstitute.org

Mary Redwine
Administrative Lab Coordinator
MRedwine@buckinstitute.org
Phone: 415-209-2237

One of the interests of the lab lays in studying how different Aβ aggregates can induce cellular senescence in brain cells. In the video, a 3D reconstruction of immunocytochemistry for neuron marker (MAP2, violet), astrocyte marker (GFAP, green), and amyloid beta markers for oligomers A11 (turquoise) as well as monomers, oligomers, protofibrils, and mature fibrils MOAB2 (red).

Amyloid beta (Aβ) is a fragment of the amyloid precursor protein (APP) and is the major constituent of senile plaques, one of the hallmarks of Alzheimer’s disease (AD), as well as other toxic aggregates such as oligomers and protofibrils. Aβ aggregates are thought to trigger a cascade of events that lead to clinical AD years to decades after they first appear. How this cascade works is still a mystery to science and understanding it may hold the key to stopping AD. At the Andersen lab we think Aβ aggregates trigger a process called cellular senescence. Cellular senescence is routinely studied outside the brain as an oncosuppressive mechanism. When unchecked, cellular senescence is thought to be a driver of aging and age-related disease. Unlike the vast majority of organs, the brain is not equipped to resolve cellular senescence, making it susceptible to the accumulation of senescent cells for years. At the Andersen lab we are researching a cellular senescence as a normal physiological process taking place in the wrong place: a “a failure in the design” that may ultimately result in AD.

Selected Publications
  • Lee S, Wang EY, Steinberg AB, Walton CC, Chinta SJ, Andersen JK. A guide to senolytic intervention in neurodegenerative disease. Mech Ageing Dev. 2021 Oct 7:111585. doi: 10.1016/j.mad.2021.111585. Online ahead of print.PMID: 34627838

  • Verma DK, Seo BA, Ghosh A, Ma SX, Hernandez-Quijada K, Andersen JK, Ko HS, Kim YH. Alpha-Synuclein Preformed Fibrils Induce Cellular Senescence in Parkinson’s Disease Models. Cells. 2021 Jul 5;10(7):1694. doi: 10.3390/cells10071694.PMID: 34359864 

  • Schmidt MY, Chamoli M, Lithgow GJ, Andersen JK. Swimming exercise reduces native ⍺-synuclein protein species in a transgenic C. elegans model of Parkinson’s disease. MicroPubl Biol. 2021 Jun 29;2021:10.17912/micropub.biology.000413. doi:10.17912/micropub.biology.000413.PMID: 34222835 

  • Chinta SJ, Woods G, Demaria M, Rane A, Zou Y, McQuade A, Rajagopalan S, Limbad C, Madden DT, Campisi J, Andersen JK (2018). Cellular senescence is induced by the environmental neurotoxin paraquat and contributes to neuropathology linked to Parkinson’s disease. Cell Rep. 22: 930-940.
  • Woods G, Andersen JK (2018). Screening method for identifying toxicants capable of inducing astrocyte senescence. Toxicol Sci. doi: 10.1093/toxsci/kfy181. PMCID:  PMC6204767.
  • Andersen JK (2018). Neurodegeneration. Innovation in Aging. 2018 Nov; 2 (Suppl 1): 745.   
  • Rane A, Rajagopalan S, Ahuja M, Thomas B, Chinta SJ, Andersen JK (2019). Hsp90 Co-chaperone p23 contributes to dopaminergic mitochondrial stress via stabilization of PHD2: Implications for Parkinson’s disease. Neurotoxicology 65: 166-173.
  • Tom S, Rane A, Katewa AS, Chamoli M, Matsumoto RR, Andersen JK, Chinta SJ. (2019).   Gedunin Inhibits Oligomeric Aβ1-42-Induced Microglia Activation Via Modulation of Nrf2-NF-κB Signaling. Mol Neurobiol. 56: 7851-7862.
  • Walton CC, Begelman D, Nguyen W, Andersen JK (2020) Senescence as an Amyloid  Cascade: The Amyloid Senescence Hypothesis. Front Cell Neurosci. 2020 May 19;14:129.
  • Chamoli M, Chinta SJ, Andersen JK, Lithgow GJ. (2020) Kavain suppresses Human Aβ-induced Paralysis in C. elegans. MicroPubl Biol.
  • Anand N, Holcom A, Broussalian M, Schmidt M, Chinta SJ, Lithgow GJ, Andersen JK*, Chamoli M*. (2020). Dysregulated iron metabolism in C. elegans catp-6/ATP13A2 mutant impairs mitochondrial function. *co-senior authors. Neurobiol. Dis.  
  • Viel T, Chinta S, Rane A, Chamoli M, Buck H, Andersen JK (2020) Microdose lithium reduces cellular senescence in human astrocytes – a potential pharmacotherapy for COVID-19? Aging. 103449. Volume 12, Issue 11, pp10035-10040.
  • Evans DS, O’Leary M, Andersen JK, et al (2021) Longitudinal Functional Study of Murine Aging: A Resource for Future Study Designs. JBMR Plus. Doi: 10.1002/jbm4.10466.

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