Investigating molecular mechanisms of Healthy aging

By 2030 almost every fourth person will be 65 or older in Switzerland, Europe, and USA. Since old age is the main risk factor for developing cancer, neurodegenerative, cardiovascular, and metabolic diseases, as well as other age-related pathologies, the growing elderly population poses an immense social and financial challenge. [read more] [pdf]

Using C. elegans as a pioneering system to model the aging process because of its ease for genetic manipulation, high evolutionary conservation of genes implicated in human diseases, and short lifespan (3 weeks). Importantly, using C. elegans lifespan assays as a read-out for extension of healthspan is a tractable and fast approach for discovering novel mechanisms that confer healthy aging. Several fundamental mechanisms discovered in C. elegans have been shown to delay age-related pathologies in higher organisms, such as mice, and these mechanisms have major implications for humans aging. Hence, by using C. elegans to model the aging process we could rapidly identify strategies to improve human healthspan.

Our recent work has shown that many health- and longevity-promoting interventions re-activate the expression of extracellular matrix (ECM) genes during aging (Ewald et al., Nature 2015, PMID:25517099). This ECM enhancement is required and sufficient for extending the lifespan of C. elegans. Our research efforts are focusing on exploring the mechanism(s) of how prolonged ECM homeostasis promotes healthy aging. [read more] [pdf]

Our core competencies are:

1. Aging research
2. Extracellular matrix biology
3. Molecular biology, genetics, and neuroscience

Our technical expertise with using the model organism C. elegans are:

• Automated lifespan assessment using the lifespan machine.
• High-throughput screening with genetic manipulations and chemical compounds for aging research.
• Neuronal plasticity (learning) assays.

• No animal safety or ethical issues: For FSVO, C. elegans not defined as an animal
• 60-80% of genes conserved with humans
• multicellular and eukaryotic
• C. elegans ages similar to humans, but faster (lifespan of 3 weeks)
• scalable for high-throughput genetic and drug screens

Wir alle werden älter und mit jedem zusätzlichen Jahr steigt das Risiko für den
Ausbruch einer altersbedingten Krankheit wie Krebs, Diabetes, Alzheimer oder
Herzkreislaufprobleme. [weiter lesen] [pdf]

Wenn Sie mehr wissen wollen, meine Einführungsvorlesung an der ETH Zürich gibt eine gute Übersicht über unsere Forschung.

Videolink zur Einführungsvorlesung

Auf den Link klicken und die Vorlesung: "Molekulare Mechanismen des gesunden Alterns (Collin Ewald)" kommen.

Welcome to the (Extracellular) Matrix: An interview with Dr. Collin Ewald - Geroscience

Ep. 3 - Prof. Collin Ewald talks getting old and feeling young - Part 1 | Simplifyd

Ep. 3 - Prof. Collin Ewald talks the cost of Alzheimer's and "mega cancer"- Part 2 | Simplifyd

An almost forgotten pioneer - UNI NOVA

Ewald Lab Logo designed by Felix Marbet: http://felixmarbet.strikingly.com​

www.ssfar.ch

www.ssmb.ch

We are a member of the GENiE network that connects young research labs across Europe that work with the model organism C. elegans. Link to our GENiE profile.

We are a member of the Molecular Life Science PhD program at the ETH Zurich and the University of Zurich Life Science Zurich Graduate School.

We use Benchling. Ewald Lab profile on Benchling. Our recent protocol on Benchling.

C. elegans

Sydney Brenner (1974) The Genetics of Caenorhabditis elegans.

Corsi, A.K., et al. 2015. A Transparent Window into Biology: A Primer on Caenorhabditis elegans. Genetics. 2015 Jun;200(2):387-407. doi: 10.1534/genetics.115.176099.

Jorgensen, E.M. & Mango, S.E., 2002. The art and design of genetic screens: Caenorhabditis elegans. Nature Reviews Genetics, 3(5), pp.356–369.

Aging Research

Kenyon, C.J. et al., 1993. A C. elegans mutant that lives twice as long as wild type. Nature, 366(6454), pp.461–464.

Herndon, L.A. et. al., 2002. Stochastic and genetic factors influence tissue-specific decline in ageing C. elegans. Nature. 24;419(6909):808-14.

Gidalevitz, T. et al., 2006. Progressive disruption of cellular protein folding in models of polyglutamine diseases. Science (New York, NY), 311(5766), pp.1471–1474.

Kenyon, C.J., 2010. The genetics of ageing. Nature, 464(7288), pp.504–512.

López-Otín, C. et al., 2013. The hallmarks of aging. Cell, 153(6), pp.1194–1217.

Taylor, R.C. et al., 2014. Systemic stress signalling: understanding the cell non-autonomous control of proteostasis. Nature Reviews Molecular Cell Biology, 15(3), pp.211–217.

Mannick, J.B. et al., 2014. mTOR inhibition improves immune function in the elderly. Science translational medicine, 6(268), pp.268ra179–268ra179.

Scott, C.T., 2015. Selling long life. Nat Biotechnol. 2015 Jan;33(1):31-40. doi: 10.1038/nbt.3108.

Advice for young researchers

Kahn, C.R., 1994. Picking a research problem. The critical decision. The New England journal of medicine, 330(21), pp.1530–1533.

Alon, U., 2009. How to choose a good scientific problem. Molecular cell, 35(6), pp.726–728.

Lindquist, S., 2010. Three quite different things that matter to me. Molecular biology of the cell, 21(22), pp.3804–3804.

Martin Chalfie. 2014. The Secret to Getting the Postdoc You Want

Peter Walter: On Careers and 42

Mensh, B. & Kording, K., 2017. Ten simple rules for structuring papers. PLoS Computational Biology, 13(9), p.e1005619.

Most beautiful presented papers

Yip, Z.C. & Heiman, M.G., 2016. Duplication of a Single Neuron in C. elegans Reveals a Pathway for Dendrite Tiling by Mutual Repulsion. Cell reports, 15(10), pp.2109–2117.

Additional Resources:

The Elements of Style by William Strunk, Jr.

WormAtlas

WormBook

C. elegans II, 2nd edition

The Worm Breeder's Gazette

WormBase

WormClassroom

ApE- A plasmid Editor

The illustrated guide to a Ph.D.

Is It Real? Can We Win? Is It Worth Doing?: Managing Risk and Reward in an Innovation Portfolio