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Title: Disease, Werner-His

Disease, Werner-His: Named for the German physician Heinrich Werner (who did not describe Werner's premature aging syndrome) and the Swiss physician Wilhelm His, Jr. (who did describe the bundle of His in the heart), this is a louse-borne disease that was first recognized in the trenches of World War I and so was called trench fever. It is caused by Bartonella quintana. Werner-His disease (trench fever) is estimated to have affected more than a million people in Russia and on the war fronts in Europe. Trench fever was again a major problem in the military in World War II and is seen endemically in Mexico, Africa, E. Europe, and elsewhere. Urban trench fever occurs among the homeless people and people with alcoholism today. Outbreaks have been documented, for example, in Seattle, Baltimore (among injection-drug users), Marseilles (France) and Burundi. The cause of trench fever is Bartonella quintana (also called Rochalimaea quintana), an unusual rickettsial organism that multiplies in the gut of the body louse. Transmission of the rickettsia to people can occur by rubbing infected louse feces into abraded (scuffed) skin or into the conjunctivae (whites of the eyes). The disease is classically a 5-day fever. The onset of symptoms is sudden with high fever, severe headache, back pain and leg pain and a fleeting rash.

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Question: What came first, the accelerated aging or the cancer?

Book by David Sinclair: https://amzn.to/3tkvX9l

References:
Centenarian study: https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC47123

Horvath clock original paper: https://genomebiology.biomedce....ntral.com/articles/1

Erosion of the epigenetic landscape: https://www.biorxiv.org/content/10.1101/808642v1

Information to Werner Syndrome: https://en.wikipedia.org/wiki/Werner_syndrome

Exciting studies on longevity:
- https://www.nature.com/articles/s41586-020-2975-4

- https://pubmed.ncbi.nlm.nih.gov/19041753/

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Did you know that your genes can be switched on and off? They can, and while this is mostly okay, it's also one of the reasons we age—and we just might be able to do something about it.

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Sources & further reading:

The hallmarks of aging:
López-Otín, C., Blasco, M. A., Partridge, L., Serrano, M., & Kroemer, G. (2013). The hallmarks of aging. Cell, 153(6), 1194-1217. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC38361

Influence of smoking on epigenetics:
Lee, K. W., & Pausova, Z. (2013). Cigarette smoking and DNA methylation. Frontiers in genetics, 4, 132. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC37132

Talikka, M., Sierro, N., Ivanov, N. V., Chaudhary, N., Peck, M. J., Hoeng, J., ... & Peitsch, M. C. (2012). Genomic impact of cigarette smoke, with application to three smoking-related diseases. Critical reviews in toxicology, 42(10), 877-889. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC34914

Knopik, V. S., Maccani, M. A., Francazio, S., & McGeary, J. E. (2012). The epigenetics of maternal cigarette smoking during pregnancy and effects on child development. Development and psychopathology, 24(4), 1377-1390. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC35810

Influence of chronic stress on epigenetics:
Hunter, R. G. (2012). Epigenetic effects of stress and corticosteroids in the brain. Frontiers in cellular neuroscience, 6, 18. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC33298

Cunliffe, V. T. (2016). The epigenetic impacts of social stress: how does social adversity become biologically embedded?. Epigenomics, 8(12), 1653-1669. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC52890

Rusconi, F., & Battaglioli, E. (2018). Acute stress-induced epigenetic modulations and their potential protective role toward depression. Frontiers in molecular neuroscience, 11, 184. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC59906

Chromatin remodeling and transcriptional alterations in progeroid syndromes:
Oberdoerffer, P., & Sinclair, D. A. (2007). The role of nuclear architecture in genomic instability and ageing. Nature reviews Molecular cell biology, 8(9), 692. (https://www.nature.com/articles/nrm2238)

Epigenetic changes in aging:
Kane, A. E., & Sinclair, D. A. (2019). Epigenetic changes during aging and their reprogramming potential. Critical reviews in biochemistry and molecular biology, 54(1), 61-83. (https://www.tandfonline.com/do....i/abs/10.1080/104092

Euchromatin and heterochromatin in progeroid syndromes and aging:
Zhang, W., Li, J., Suzuki, K., Qu, J., Wang, P., Zhou, J., ... & Yuan, T. (2015). A Werner syndrome stem cell model unveils heterochromatin alterations as a driver of human aging. Science, 348(6239), 1160-1163. (https://www.ncbi.nlm.nih.gov/p....mc/articles/PMC44946

Scaffidi, P., & Misteli, T. (2006). Lamin A-dependent nuclear defects in human aging. Science, 312(5776), 1059-1063. (https://www.ncbi.nlm.nih.gov/pubmed/16645051)

Partial cellular reprogramming with OSKM:
Ocampo, A., Reddy, P., Martinez-Redondo, P., Platero-Luengo, A., Hatanaka, F., Hishida, T., ... & Araoka, T. (2016). In vivo amelioration of age-associated hallmarks by partial reprogramming. Cell, 167(7), 1719-1733. (https://www.cell.com/fulltext/....S0092-8674(16)31664-

Alternative partial cellular reprogramming approach by Turn.Bio:
Sarkar, T. J., Quarta, M., Mukherjee, S., Colville, A., Paine, P., Doan, L., ... & Rando, T. A. (2019). Transient non-integrative nuclear reprogramming promotes multifaceted reversal of aging in human cells. bioRxiv, 573386. (https://www.biorxiv.org/conten....t/10.1101/573386v1.f

https://www.leafscience.org/an-interview-with-prof-vittorio-sebastiano-of-turn-bio/ https://www.leafscience.org/partial-cellular-reprogramming-to-reverse-cellular-aging/
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PART 2 : https://youtu.be/iFMQW86BnAk
PART 3 : https://youtu.be/Hl1N5Nbi5sU
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Richard Faragher, University of Brighton, UK, presents at the 2020 Aging Research and Drug Discovery conference.

About the Aging Research and Drug Discovery meeting:
According to the United Nations, the proportion of people aged over 65 now outnumber children younger than 5. The enormous growth in the elderly population is posing a socioeconomic challenge to societies worldwide, and necessitates new sweeping interventions for age-associated diseases. This year we have an incredibly exciting program with global thought-leaders sharing their latest insights into aging and how we target aging process ensuring everyone lives a healthier and longer life. Welcome to the 7th Aging Research and Drug Discovery Meeting.

Read more on:
www.agingpharma.org