The Cancer Chronicles: Unlocking Medicine's Deepest Mystery
by George Johnson · 26 Aug 2013 · 465pp · 103,303 words
so much like a tumor: The complex process of implantation is described in Haibin Wang and Sudhansu K. Dey, “Roadmap to Embryo Implantation: Clues from Mouse Models,” Nature Reviews Genetics 7, no. 3 (March 1, 2006): 185–99. [http://www.nature.com/nrg/journal/v7/n3/abs/nrg1808.html] For some of
Lifespan: Why We Age—and Why We Don't Have To
by David A. Sinclair and Matthew D. Laplante · 9 Sep 2019
in Cell Biology 27, no. 9 (September 27, 2017): 685–96, https://www.ncbi.nlm.nih.gov/pubmed/28528987. 15. D. C. Dolinoy, “The Agouti Mouse Model: An Epigenetic Biosensor for Nutritional and Environmental Alterations on the Fetal Epigenome,” Nutrition Reviews 66, suppl. 1 (August 2008): S7–11, https://www.ncbi.nlm
CRISPR People: The Science and Ethics of Editing Humans
by Henry T. Greely · 22 Jan 2021
Johnston, “Embryology Policy: Revisit the 14-Day Rule,” Nature 533, no. 7602 (2016): 169–171, https://doi.org/10.1038/533169a. 14. Robert L. Perlman, “Mouse Models of Human Disease: An Evolutionary Perspective,” Evolution, Medicine, and Public Health 2016, no. 1 (January 2016), https://doi.org/10.1093/emph/eow014. 15. David
She Has Her Mother's Laugh
by Carl Zimmer · 29 May 2018
generation of graduate students silently thanked Jaenisch every day for making their lives easier. Many PhD projects had to start with the creation of a mouse model to study a gene or a disease. It typically took eighteen months to create a line of mice, and often it took more than one
Junk DNA: A Journey Through the Dark Matter of the Genome
by Nessa Carey · 5 Mar 2015 · 357pp · 98,853 words
more sawdust you create. But researchers managed to find a way of specifically decreasing the expression of just the long non-coding RNA in a mouse model which frequently develops Alzheimer’s pathology. The knockdown of the long non-coding RNA resulted in decreased BACE1 protein and fewer beta-amyloid plaques. This
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base. The researchers who identified the C to T change in the enhancer did exactly this, by testing the effect of this change in a mouse model. They showed that when the C was present, this stretch of junk DNA acted as an enhancer of morphogen expression. But when the C was
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animals. Spatial memory was better and the mice behaved appropriately around other mice. They were also less susceptible to seizures than the standard Fragile X mouse models. These symptomatic improvements were consistent with underlying changes that the scientists detected in the brains of the animals.14 Neurons in normal brains have little
Ageless: The New Science of Getting Older Without Getting Old
by Andrew Steele · 24 Dec 2020 · 399pp · 118,576 words
, but staying younger for longer, with fewer and less severe age-related diseases. Rapamycin slows cell death and improves cognitive performance in the brains of mouse models* of Parkinson’s and Alzheimer’s, and improves the functioning of arteries in diabetic mice, probably by stimulating autophagy. This is an impressive proof of
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the 1990s). It’s hard to overemphasise how bizarre this is, but nonetheless GAIM has been shown to clear both amyloid beta and tau in mouse models of Alzheimer’s disease, and to improve their cognitive function. Human trials are ongoing, headed up by a company called Proclara Biosciences. Ideally, one or
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chemical secreted by the mould which was toxic to bacteria – eventually isolated and named penicillin after the Penicillium fungus in which it was discovered. *A ‘mouse model’ is what scientists call mice genetically modified to be at risk of a human disease, either because waiting around for them to get it would
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it’s often a vital first step in understanding how new treatments work. Nonetheless, bear in mind both in this book and elsewhere that a mouse model is one step further removed from the clinic than an experiment in normal mice might be. *Spermidine and related compound spermine were first observed by
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as SLAB51 was able to damp inflammation, reduce beta-amyloid and tau aggregation, reduce levels of advanced glycation end products and slow cognitive decline in mouse models of Alzheimer’s. Probiotics, prebiotics and synbiotics have also been successfully used in small human trials to improve symptoms in Alzheimer’s and control sugar
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risk of cancer in old mice, slow the progression of age-related heart problems, reduce the production of amyloid-beta and extend the lives of mouse models of Alzheimer’s, and improve muscle function in old mice. There are also several mitochondrially targeted antioxidant drugs in the works. Probably the most advanced
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found in our food, which has been shown to extend lifespan in worms, improve endurance and muscle strength in mice and slow cognitive decline in mouse models of Alzheimer’s, as well as improve mitochondrial function in people over 60. Other contenders for mitophagy-boosting include spermidine, one of the DR mimetics
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. There should be a similar refrain in geriatrics, that old people aren’t just old young people. The same problem plays out in mouse studies. ‘Mouse models’ of disease – which we’ve said before are often imperfect analogues – are particularly guilty in this regard. For example, a
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mouse model of Alzheimer’s might contain an extra copy of the amyloid precursor protein gene, and mice could develop amyloid deposits and cognitive impairment in mouse
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after your mice for a year or two while they grow old. However, it’s well known that lots of drugs which work flawlessly in mouse models fail to translate to human success. If your drug is for a disease primarily found in older patients, this is one of many possible reasons
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ageless.link/o44mop A probiotic cocktail … known as SLAB51 … Laura Bonfili et al., ‘Gut microbiota manipulation through probiotics oral administration restores glucose homeostasis in a mouse model of Alzheimer’s disease’, Neurobiol. Aging 87, 35–43 (2019). DOI: 10.1016/j.neurobiolaging.2019.11.004 ageless.link/jjwfum Probiotics, prebiotics and synbiotics
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/voxv4s … reduce the production of amyloid-beta … Peizhong Mao et al., ‘Mitochondria-targeted catalase reduces abnormal APP processing, amyloid β production and BACE1 in a mouse model of Alzheimer’s disease: Implications for neuroprotection and lifespan extension’, Hum. Mol. Genet. 21, 2973–90 (2012). DOI: 10.1093/hmg/dds128 ageless.link/divufs
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microbiome, here, here heart rate, here and immune system therapies, here, here, here and longevity genes, here, here, here mitochondria, here and mitochondrial therapies, here mouse models, here and p53 gene, here and parabiosis, here, here, here and plasma transfusions, here and senescent cell research, here and stem cells, here, here, here
Food Allergy: Adverse Reactions to Foods and Food Additives
by Dean D. Metcalfe · 15 Dec 2008 · 623pp · 448,848 words
epicutaneous sensitized mice to the egg protein OVA [38]. The dose of antigen administered is also critical to the form of oral tolerance generated. In mouse models, low doses of antigen appear to activate regulatory/suppressor T-cells [39,40]. There are an increasing number of such cells identified, of both CD4
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activities are broad and non-specific. A recent investigation of the adaptive immune response to cholera toxin B subunit and macrophage-activating lipopeptide-2 in mouse models lacking the TGF-βR in B-cells (TGFβRII-B) demonstrated undetectable levels of antigen-specific IgA-secreting cells, serum IgA, and secretory IgA (SIgA) [46
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well defined. Tr1 cells produce interleukin (IL)-10 and appear to be involved in the suppression of graft-versus-host disease (GVHD) and colitis in mouse models, but their activation during oral antigen administration has not been as clearcut [47–49]. Frossard et al. demonstrated increased antigen induced IL-10 producing cells
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of soluble antigen [102]. More recent data demonstrate that tolerance can occur in the absence of M-cells and PPs. Kraus et al. created a mouse model of surgically isolated small bowel loops (fully vascularized with intact lymphatic drainage) that either contained or were deficient in M-cells and PPs. They were
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cells. Gastroenterology 1990;98:56–8. 96 Frossard CP, Hauser C, Eigenmann PA. Antigen-specific secretory IgA antibodies in the gut are decreased in a mouse model of food allergy. J Allergy Clin Immunol 2004;114:377–82. 97 Kerneis S, Bogdanova A, Kraehenbuhl JP, Pringault E. Conversion by Peyer’s patch
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2001;166:7282–9. 116 Man AL, Bertelli E, Regoli M, et al. Antigen-specific T cellmediated apoptosis of dendritic cells is impaired in a mouse model of food allergy. J Allergy Clin Immunol 2004;113:965–72. 121 Hershberg RM, Mayer LF. Antigen processing and presentation by intestinal epithelial cells – polarity
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a considerable role in the defense against helminthes. This is supported by findings in both humans and animal models [28,124]. Recently, two eosinophil-deficient mouse models have been developed. In both strains, eosinophils substantially impact on experimental allergic asthma, but apart from this common finding, they give divergent results. While the
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, which despite functional downregulation have conserved their ability to secrete certain cytokines, such as IL-10 and TGFβ. Oral tolerance in humans: How well do mouse models mimic the human situation? As noted above, the baseline “default” response of laboratory mice appears biased toward a Th2-like cytokine profile, admixed with TGFβ
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), and egg (one patient) [6]. Several authors have suggested that aeroallergens may play a role in the development of EoE. Mishra and Rothenberg used a mouse model to show that the inhalation of Aspergillus may cause EoE [7]. They found that the allergenchallenged mice developed elevated levels of esophageal eosinophils and features
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[101]. Presence of IgE in the mucosal biopsies was reported by two groups but was not confirmed in large series of infants [113]. In a mouse model of allergic enteropathy, evidence of local Figure 16.1 Biopsy of duodenal mucosa obtained from a 6-monthold infant with cow’s milk-protein-induced
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sheep red blood cells would be expected to do. Bashir et al. examined the impact of TLR4 deficiency on oral sensitization to peanut in a mouse model of anaphylaxis Experimental Approaches to the Study of Food Allergy [54]. They found that TLR4 deficiency was associated with susceptibility to peanut sensitization and associated
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Clin Immunol 2004;114:915–21. 15 Frossard CP, Hauser C, Eigenmann PA. Antigen-specific secretory IgA antibodies in the gut are decreased in a mouse model of food allergy. J Allergy Clin Immunol 2004;114:377–82. 16 Frossard CP, Tropia L, Hauser C, Eigenmann PA. Lymphocytes in Peyer patches regulate
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. Gastroenterology 2005;128:825–32. 98 Kim H, Kwack K, Kim DY, Ji GE. Oral probiotic bacterial administration suppressed allergic responses in an ovalbumininduced allergy mouse model. FEMS Immunol Med Microbiol 2005;45:259–67. 88 Li XM, Srivastava K, Huleatt JW, et al. Engineered recombinant peanut protein and heat-killed Listeria
A Crack in Creation: Gene Editing and the Unthinkable Power to Control Evolution
by Jennifer A. Doudna and Samuel H. Sternberg · 15 Mar 2017
the earliest and most dramatic demonstrations that CRISPR can ameliorate the ravaging effects of genetic disease in vivo. While the technique was demonstrated in a mouse model, there’s every reason to think that it will be effective in human subjects as well—not least because the genetic disease it was used
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. In humans, the disease can cause an accumulation of toxic metabolites and extensive liver damage; if untreated, patients usually die before age ten. In the mouse model, however, CRISPR repaired the damaged gene and reversed the course of the disease. AAV has also delivered CRISPR into the brains of adult mice, into
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was rather limited: scientists could detect and diagnose mutations in biopsies taken from patients, and they could study a small number of discrete mutations in mouse models. But now that researchers have a way to precisely replicate cancer-causing mutations—single ones, or many at a time—in a fraction of the
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research is poised to explode. Instead of painstakingly selecting the correctly mutated cells (an ordeal with one-in-a-million efficiencies) or breeding the desired mouse models over numerous generations (requiring years of time), scientists can use CRISPR to efficiently introduce mutations in a single pass. This capability is allowing scientists to
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, from cloning to virus-based gene addition to the earliest uses of precision gene editing. By the 1990s, it had become fairly routine to generate mouse models of human disease by modifying specific genes in the mouse germline; although the exact procedure couldn’t be used on humans, it set the stage
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, Cancer Facts and Figures 2016 (Atlanta: American Cancer Society, 2016). to understand the genetic causes of acute myeloid leukemia: D. Heckl et al., “Generation of Mouse Models of Myeloid Malignancy with Combinatorial Genetic Lesions Using CRISPR-Cas9 Genome Editing,” Nature Biotechnology 32 (2014): 941–46. one of the first to pioneer such
P53: The Gene That Cracked the Cancer Code
by Sue Armstrong · 20 Nov 2014 · 260pp · 84,847 words
in which various tumour suppressors had been deleted and he was asking the simple and obvious question: do the animals get cancer? He had a mouse model with p53 knocked out, but he had been beaten to it in his experiments by another scientist who had been investigating the same question, so
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independently and wondered about – death among their oncogene-driven cells – were caused by the oncogenes switching on tumour suppressors, frequently p53. The multiple experiments with mouse models – knocking out p53 altogether, or else toggling the gene back and forth between active and passive – made it very clear that this is an extremely
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and sending in the repair team; condemning it to permanent arrest or senescence; or forcing it to commit suicide. Another researcher, Gigi Lozano, working with mouse models at MD Anderson Cancer Center in Houston, confirmed just how important each protein is to the normal functioning of the other in real life when
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Baker and Bert Vogelstein in Baltimore revealed that wild-type p53 was in fact a tumour suppressor, and later that same year scientists working with mouse models in Toronto published a paper describing the multiple tumour types that developed in animals with mutant p53. The constellation of mouse tumours didn’t exactly
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created transgenic mice to try to resolve it and to find out what happens in real life. Guillermina (‘Gigi’) Lozano, whom we met working with mouse models at MD Anderson in Houston in Chapter 13, headed one such group. Lozano’s family had immigrated to the US from Mexico in search of
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job in molecular genetics at MD Anderson, where she is now Professor and Head of the Department of Cancer Genetics. Much of her research involves mouse models and in the early 2000s she set about creating one that mimics the human Li-Fraumeni syndrome, in which the p53 gene has one wild
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for creating one of the two first p53 knock-out mice in 1992 – was on the same track. His lab was busy generating two different mouse models that mimicked LFS – one with the same point mutation as Lozano’s mice, corresponding to human R175H, and another corresponding to R273H. The two groups
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published their findings in the same edition of Cell in December 2004. What distinguished their mouse models from others designed to test the activity of mutant p53 was that here the gene was being switched on naturally in response to signals from
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more than simply hobble the wild-type allele and shut down its protective functions – clearly it had a life of its own. These and other mouse models have allowed researchers gradually to build a picture of how the mutants work and how they interact with wild-type p53. Context, it seems, is
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Heidi Scrable of the University of Virginia at Charlottesville, provided new evidence that Donehower’s original hunch was right. She and her team created a mouse model in which the only change to its DNA was the replacement of one allele of p53 with a naturally occurring hyperactive version of the gene
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with every aspect of tumour suppression, context is all important: different cell types and tissues follow different paths on activation of p53. Scott Lowe, another mouse-model man, whom we met in the chapter on apoptosis, is also at the cutting edge of cell-senescence research; he discovered that, although these cells
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in response to damage of their DNA – the normal response to cell stress, mediated by p53. Scott Lowe, whom we met in Chapter 12 creating mouse models and making groundbreaking discoveries about apoptosis and p53, was one of the first to recognise the tumour suppressor’s central role in conventional therapy. To
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. EVAN, GERARD A scientist with Cancer Research UK (CRUK), now based at Cambridge University as Professor of Biochemistry. An early enthusiast for the use of mouse models to find out how things work in living organisms, he is renowned as an original thinker whose work frequently challenges mainstream thinking. We meet him
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simultaneously in the same journal, Cell, Volume 119, 2004, by Tyler Jacks and Gigi Lozano and their colleagues: ‘Mutant p53 Gain of Function in Two Mouse Models of Li-Fraumeni Syndrome’ by Kenneth P Olive et al. (847–860) and ‘Gain of Function of a p53 Hot Spot Mutation in a
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Mouse Model of Li-Fraumeni Syndrome’ by Gene A Lang et al. (861–872). See also ‘Mutant p53: one name, many proteins’ by William A. Freed-Pastor
In Pursuit of Memory: The Fight Against Alzheimer's
by Joseph Jebelli · 30 Oct 2017 · 294pp · 87,429 words
, studies also found that screening drugs in mice was far from ideal. In 2010 it was estimated that 90 per cent of drugs based on mouse models fail in clinical trials.5 The reason: unlike mice found in the wild, lab mice are inbred, and therefore don’t capture the huge genetic
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sunroofs, and the larger picture would be substantially missed’.6 Indeed, one study found that only 12 per cent of the genetic changes seen in mouse models of inflammatory disorders mimicked those seen in humans7–providing ‘a sobering reminder’, wrote an editor for Nature Methods, ‘of what most thoughtful biologists already know
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Higgins, ‘Alzheimer’s disease’. 3. Games, Adams, et al., ‘Alzheimer-type neuropathology in transgenic mice overexpressing V717F beta-amyloid precursor protein’. 4. Duff and Hardy, ‘Mouse model made’. 5. Saunders, Strittmatter, et al., ‘Association of apolipoprotein E allele epsilon 4 with late-onset familial and sporadic Alzheimer’s disease’. 6. Roses, ‘On
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reliably inform human studies?’. 6. Warren, Tompkins, et al., ‘Mice are not men’. 7. Seok, Warren, et al., ‘Genomic responses in mouse models poorly mimic human inflammatory diseases’. 8. De Souza, ‘Mouse model challenged’. 9. Choi, Kim, et al., ‘A three-dimensional human neural cell culture model of Alzheimer’s disease’. 10. Hallett, Cooper
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/conference-coverage/two-faces-evil-cancer-and-neurodegeneration 4. Cramer, Cirrito, et al., ‘ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models’. 5. Stamps, Bartoshuk, Heilman, ‘A brief olfactory test for Alzheimer’s disease’. 6. Wang, ‘Alzheimer’s families clamor for drug’. 7. Pierrot, Lhommel, et al
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. W., Lee, C. Y., Karlo, J. C., Zinn, A. E.,… Landreth, G. E., ‘ApoE-directed therapeutics rapidly clear beta-amyloid and reverse deficits in AD mouse models’, Science, 335 (6075), 2012, 1503–6 Crutch, S. J., Lehmann, M., Schott, J. M., Rabinovici, G. D., Rossor, M. N., Fox, N. C., ‘Posterior cortical
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, 2016 De Grey, A., Ending Aging: The Rejuvenation Breakthroughs That Could Reverse Human Aging in Our Lifetime, St Martin’s Griffin, 2008 De Souza, N., ‘Mouse model challenged’, Nature Methods, 10 (4), 2013, 288 De Strooper, B., and Karran, E., ‘The cellular phase of Alzheimer’s disease’, Cell, 164 (4), 2016, 603
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. C., ‘Of mice and men: what rodent models don’t tell us’, Cellular & Molecular Immunology, 10 (4), 2013, 284–5 Duff, K., and Hardy, J., ‘Mouse model made’, Nature, 373 (6514), 1995, 476–7 Eisele, Y. S., Obermüller, U., Heilbronner, G., Baumann, F., Kaeser, S. A., Wolburg, H.,… Jucker, M., ‘Peripherally applied
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, H. S., Cuenca, A. G., Mindrinos, M. N., Baker, H. V., Xu, W.,… Host Response to Injury, L. S. C. R. P., ‘Genomic responses in mouse models poorly mimic human inflammatory diseases’, Proceedings of the National Academy of Sciences of the United States of America, 110 (9), 2013, 3507–12 Sepulveda-Falla
The Death of Cancer: After Fifty Years on the Front Lines of Medicine, a Pioneering Oncologist Reveals Why the War on Cancer Is Winnable--And How We Can Get There
by Vincent T. Devita, Jr., M. D. and Elizabeth Devita-Raeburn · 3 Nov 2015 · 386pp · 114,405 words
Behave: The Biology of Humans at Our Best and Worst
by Robert M. Sapolsky · 1 May 2017 · 1,261pp · 294,715 words
Grain Brain: The Surprising Truth About Wheat, Carbs, and Sugar--Your Brain's Silent Killers
by David Perlmutter and Kristin Loberg · 17 Sep 2013
The Emperor of All Maladies: A Biography of Cancer
by Siddhartha Mukherjee · 16 Nov 2010 · 1,294pp · 210,361 words
The Gene: An Intimate History
by Siddhartha Mukherjee · 16 May 2016 · 824pp · 218,333 words
Sleepyhead: Narcolepsy, Neuroscience and the Search for a Good Night
by Henry Nicholls · 1 Mar 2018 · 367pp · 102,188 words
Potatoes not Prozac
by Kathleen DesMaisons, Ph. D. · 265pp · 75,669 words
Editing Humanity: The CRISPR Revolution and the New Era of Genome Editing
by Kevin Davies · 5 Oct 2020 · 741pp · 164,057 words
Epigenetics Revolution: How Modern Biology Is Rewriting Our Understanding of Genetics, Disease and Inheritance
by Nessa Carey · 31 Aug 2011 · 357pp · 98,854 words
The Lucky Years: How to Thrive in the Brave New World of Health
by David B. Agus · 29 Dec 2015 · 346pp · 92,984 words
Immortality, Inc.
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Deep Nutrition: Why Your Genes Need Traditional Food
by Catherine Shanahan M. D. · 2 Jan 2017 · 659pp · 190,874 words
The Future of the Brain: Essays by the World's Leading Neuroscientists
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Science Fictions: How Fraud, Bias, Negligence, and Hype Undermine the Search for Truth
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The Fast Diet: Revised and Updated: Lose Weight, Stay Healthy, Live Longer
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The Science and Technology of Growing Young: An Insider's Guide to the Breakthroughs That Will Dramatically Extend Our Lifespan . . . And What You Can Do Right Now
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Exercised: The Science of Physical Activity, Rest and Health
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Why We Sleep: Unlocking the Power of Sleep and Dreams
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Practical Manual of Thyroid and Parathyroid Disease
by Asit Arora, Neil Tolley and R. Michael Tuttle · 2 Jan 2009 · 228pp · 119,593 words
Inferior: How Science Got Women Wrong-And the New Research That's Rewriting the Story
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The Code Breaker: Jennifer Doudna, Gene Editing, and the Future of the Human Race
by Walter Isaacson · 9 Mar 2021 · 700pp · 160,604 words
The Singularity Is Near: When Humans Transcend Biology
by Ray Kurzweil · 14 Jul 2005 · 761pp · 231,902 words
The Telomere Effect: A Revolutionary Approach to Living Younger, Healthier, Longer
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Hormone Repair Manual
by Lara Briden · 14 Apr 2021
The Autoimmune Connection
by Rita Baron-Faust and Jill Buyon · 21 Apr 2003 · 427pp · 30,920 words
Speculative Everything: Design, Fiction, and Social Dreaming
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The Last Best Cure: My Quest to Awaken the Healing Parts of My Brain and Get Back My Body, My Joy, a Nd My Life
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Fiber Fueled: The Plant-Based Gut Health Program for Losing Weight, Restoring Your Health, and Optimizing Your Microbiome
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Brain Energy: A Revolutionary Breakthrough in Understanding Mental Health--And Improving Treatment for Anxiety, Depression, OCD, PTSD, and More
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Betrayal of Trust: The Collapse of Global Public Health
by Laurie Garrett · 15 Feb 2000
Escape From Model Land: How Mathematical Models Can Lead Us Astray and What We Can Do About It
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Antifragile: Things That Gain From Disorder
by Nassim Nicholas Taleb · 27 Nov 2012 · 651pp · 180,162 words
The Panic Virus: The True Story Behind the Vaccine-Autism Controversy
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Warnings
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Never Bet Against Occam: Mast Cell Activation Disease and the Modern Epidemics of Chronic Illness and Medical Complexity
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The Autistic Brain: Thinking Across the Spectrum
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Autism Adulthood: Strategies and Insights for a Fulfilling Life
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Space 2.0
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The Plague Year: America in the Time of Covid
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Life on the Rocks: Building a Future for Coral Reefs
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Against Technoableism: Rethinking Who Needs Improvement
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