Full Text Journal Articles by
Author Jeremy M Van Raamsdonk

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Disruption of mitochondrial dynamics increases stress resistance through activation of multiple stress response pathways.

Emily Machiela, Thomas Liontis, Dylan J Dues, Paige D Rudich, Annika Traa, Leslie Wyman, Corah Kaufman, Jason F Cooper, Leira Lew, Saravanapriah Nadarajan, Megan M Senchuk, Jeremy M Van Raamsdonk,

Mitochondria are dynamic organelles that can change shape and size depending on the needs of the cell through the processes of mitochondrial fission and fusion. In this work, we investigated the role of mitochondrial dynamics in organismal stress response. By using C. elegans as a genetic model, we could visualize ... Read more >>

FASEB J. (FASEB journal : official publication of the Federation of American Societies for Experimental Biology)
[2020, 34(6):8475-8492]

Cited: 0 times

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Lack of consensus on an aging biology paradigm? A global survey reveals an agreement to disagree, and the need for an interdisciplinary framework.

Alan A Cohen, Brian K Kennedy, Ulrich Anglas, Anne M Bronikowski, Joris Deelen, Frédérik Dufour, Gerardo Ferbeyre, Luigi Ferrucci, Claudio Franceschi, Daniela Frasca, Bertrand Friguet, Pierrette Gaudreau, Vadim N Gladyshev, Efstathios S Gonos, Vera Gorbunova, Philipp Gut, Mikhail Ivanchenko, Véronique Legault, Jean-François Lemaître, Thomas Liontis, Guang-Hui Liu, Mingxin Liu, Andrea B Maier, Otávio T Nóbrega, Marcel G M Olde Rikkert, Graham Pawelec, Sylvie Rheault, Alistair M Senior, Andreas Simm, Sonja Soo, Annika Traa, Svetlana Ukraintseva, Quentin Vanhaelen, Jeremy M Van Raamsdonk, Jacek M Witkowski, Anatoliy I Yashin, Robert Ziman, Tamàs Fülöp,

At a recent symposium on aging biology, a debate was held as to whether or not we know what biological aging is. Most of the participants were struck not only by the lack of consensus on this core question, but also on many basic tenets of the field. Accordingly, we ... Read more >>

Mech Ageing Dev (Mechanisms of ageing and development)
[2020, 191:111316]

Cited: 1 time

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Compounds that extend longevity are protective in neurodegenerative diseases and provide a novel treatment strategy for these devastating disorders.

Sonja K Soo, Paige D Rudich, Annika Traa, Namasthée Harris-Gauthier, Hazel J Shields, Jeremy M Van Raamsdonk,

While aging is the greatest risk factor for the development of neurodegenerative disease, the role of aging in these diseases is poorly understood. In the inherited forms of these diseases, the disease-causing mutation is present from birth but symptoms appear decades later. This indicates that these mutations are well tolerated ... Read more >>

Mech Ageing Dev (Mechanisms of ageing and development)
[2020, 190:111297]

Cited: 0 times

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Resistance to Stress Can Be Experimentally Dissociated From Longevity.

Dylan J Dues, Emily K Andrews, Megan M Senchuk, Jeremy M Van Raamsdonk,

On the basis of multiple experiments demonstrating that high resistance to stress is associated with long lifespan, it has been proposed that stress resistance is a key determinant of longevity. However, the extent to which high resistance to stress is necessary or sufficient for long life is currently unclear. In ... Read more >>

J Gerontol A Biol Sci Med Sci (The journals of gerontology. Series A, Biological sciences and medical sciences)
[2019, 74(8):1206-1214]

Cited: 4 times

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Mitochondrial unfolded protein response transcription factor ATFS-1 promotes longevity in a long-lived mitochondrial mutant through activation of stress response pathways.

Ziyun Wu, Megan M Senchuk, Dylan J Dues, Benjamin K Johnson, Jason F Cooper, Leira Lew, Emily Machiela, Claire E Schaar, Heather DeJonge, T Keith Blackwell, Jeremy M Van Raamsdonk,

BACKGROUND:The mitochondrial unfolded protein response (mitoUPR) is a stress response pathway activated by disruption of proteostasis in the mitochondria. This pathway has been proposed to influence lifespan, with studies suggesting that mitoUPR activation has complex effects on longevity. RESULTS:Here, we examined the contribution of the mitoUPR to the survival and ... Read more >>

BMC Biol (BMC biology)
[2018, 16(1):147]

Cited: 6 times

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α-synuclein expression from a single copy transgene increases sensitivity to stress and accelerates neuronal loss in genetic models of Parkinson's disease.

Jason F Cooper, Katie K Spielbauer, Megan M Senchuk, Saravanapriah Nadarajan, Monica P Colaiácovo, Jeremy M Van Raamsdonk,

Parkinson's disease (PD) is the second most common neurodegenerative disease and is characterized by the formation of α-synuclein-containing protein aggregates called Lewy bodies within the brain. A crucial role for α-synuclein in the pathogenesis of PD is also suggested by the fact that point mutations, increased copy number, or polymorphisms ... Read more >>

Exp Neurol (Experimental neurology)
[2018, 310:58-69]

Cited: 7 times

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Activation of DAF-16/FOXO by reactive oxygen species contributes to longevity in long-lived mitochondrial mutants in Caenorhabditis elegans.

Megan M Senchuk, Dylan J Dues, Claire E Schaar, Benjamin K Johnson, Zachary B Madaj, Megan J Bowman, Mary E Winn, Jeremy M Van Raamsdonk,

Mild deficits in mitochondrial function have been shown to increase lifespan in multiple species including worms, flies and mice. Here, we study three C. elegans mitochondrial mutants (clk-1, isp-1 and nuo-6) to identify overlapping genetic pathways that contribute to their longevity. We find that genes regulated by the FOXO transcription ... Read more >>

PLoS Genet (PLoS genetics)
[2018, 14(3):e1007268]

Cited: 14 times

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Modeling Parkinson's Disease in C. elegans.

Jason F Cooper, Jeremy M Van Raamsdonk,

Parkinson's disease (PD) is an adult onset neurodegenerative disease that is characterized by selective degeneration of neurons primarily in the substantia nigra. At present, the pathogenesis of PD is incompletely understood and there are no neuroprotective treatments available. Accurate animal models of PD provide the opportunity to elucidate disease mechanisms ... Read more >>

J Parkinsons Dis (Journal of Parkinson's disease)
[2018, 8(1):17-32]

Cited: 14 times

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Mechanisms underlying longevity: A genetic switch model of aging.

Jeremy M Van Raamsdonk,

While the questions of "What causes aging?" and "Why do we age?" and "How can we stop it?" remain unanswered, recent advances in aging research have continued to increase our understanding of the aging process. Until the last couple of decades, aging was viewed as an inevitable process of damage ... Read more >>

Exp Gerontol (Experimental gerontology)
[2018, 107:136-139]

Cited: 4 times

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Novel animal model defines genetic contributions for neuron-to-neuron transfer of α-synuclein.

Trevor Tyson, Megan Senchuk, Jason F Cooper, Sonia George, Jeremy M Van Raamsdonk, Patrik Brundin,

Cell-to-cell spreading of misfolded α-synuclein (α-syn) is suggested to contribute to the progression of neuropathology in Parkinson's disease (PD). Compelling evidence supports the hypothesis that misfolded α-syn transmits from neuron-to-neuron and seeds aggregation of the protein in the recipient cells. Furthermore, α-syn frequently appears to propagate in the brains of ... Read more >>

Sci Rep (Scientific reports)
[2017, 7(1):7506]

Cited: 14 times

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Mitochondrial pyruvate carrier regulates autophagy, inflammation, and neurodegeneration in experimental models of Parkinson's disease.

Anamitra Ghosh, Trevor Tyson, Sonia George, Erin N Hildebrandt, Jennifer A Steiner, Zachary Madaj, Emily Schulz, Emily Machiela, William G McDonald, Martha L Escobar Galvis, Jeffrey H Kordower, Jeremy M Van Raamsdonk, Jerry R Colca, Patrik Brundin,

Mitochondrial and autophagic dysfunction as well as neuroinflammation are involved in the pathophysiology of Parkinson's disease (PD). We hypothesized that targeting the mitochondrial pyruvate carrier (MPC), a key controller of cellular metabolism that influences mTOR (mammalian target of rapamycin) activation, might attenuate neurodegeneration of nigral dopaminergic neurons in animal models ... Read more >>

Sci Transl Med (Science translational medicine)
[2016, 8(368):368ra174]

Cited: 45 times

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Oxidative stress in neurodegenerative disease: causation or association?

Jeremy M Van Raamsdonk, Irving E Vega, Patrik Brundin,

Oncotarget (Oncotarget)
[2017, 8(7):10777-10778]

Cited: 9 times

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Uncoupling of oxidative stress resistance and lifespan in long-lived isp-1 mitochondrial mutants in Caenorhabditis elegans.

Dylan J Dues, Claire E Schaar, Benjamin K Johnson, Megan J Bowman, Mary E Winn, Megan M Senchuk, Jeremy M Van Raamsdonk,

Mutations affecting components of the mitochondrial electron transport chain have been shown to increase lifespan in multiple species including the worm Caenorhabditis elegans. While it was originally proposed that decreased generation of reactive oxygen species (ROS) resulting from lower rates of electron transport could account for the observed increase in ... Read more >>

Free Radic Biol Med (Free radical biology & medicine)
[2017, 108:362-373]

Cited: 12 times

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Measuring Oxidative Stress in Caenorhabditis elegans: Paraquat and Juglone Sensitivity Assays.

Megan M Senchuk, Dylan J Dues, Jeremy M Van Raamsdonk,

Oxidative stress has been proposed to be one of the main causes of aging and has been implicated in the pathogenesis of many diseases. Sensitivity to oxidative stress can be measured by quantifying survival following exposure to a reactive oxygen species (ROS)-generating compound such as paraquat or juglone. Sensitivity to ... Read more >>

Bio Protoc (Bio-protocol)
[2017, 7(1):]

Cited: 8 times

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Oxidative stress is increased in C. elegans models of Huntington's disease but does not contribute to polyglutamine toxicity phenotypes.

Emily Machiela, Dylan J Dues, Megan M Senchuk, Jeremy M Van Raamsdonk,

Huntington's disease (HD) is an adult onset neurodegenerative disorder for which there is currently no cure. While HD patients and animal models of the disease exhibit increased oxidative damage, it is currently uncertain to what extent oxidative stress contributes to disease pathogenesis. In this work, we use a genetic approach ... Read more >>

Neurobiol. Dis. (Neurobiology of disease)
[2016, 96:1-11]

Cited: 17 times

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Aging causes decreased resistance to multiple stresses and a failure to activate specific stress response pathways.

Dylan J Dues, Emily K Andrews, Claire E Schaar, Alexis L Bergsma, Megan M Senchuk, Jeremy M Van Raamsdonk,

In this work, we examine the relationship between stress resistance and aging. We find that resistance to multiple types of stress peaks during early adulthood and then declines with age. To dissect the underlying mechanisms, we use C. elegans transcriptional reporter strains that measure the activation of different stress responses ... Read more >>

Aging (Albany NY) (Aging)
[2016, 8(4):777-795]

Cited: 32 times

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Delaying aging is neuroprotective in Parkinson's disease: a genetic analysis in C. elegans models.

Jason F Cooper, Dylan J Dues, Katie K Spielbauer, Emily Machiela, Megan M Senchuk, Jeremy M Van Raamsdonk,

Aging is the greatest risk factor for the development of Parkinson's disease (PD). However, the role of aging in the pathogenesis of PD is not known and it is currently uncertain why the symptoms take many decades to develop when inherited mutations that cause the disease can be present from ... Read more >>

(NPJ Parkinson's disease)
[2015, 1:15022]

Cited: 26 times

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Deletion of the mitochondrial superoxide dismutase sod-2 extends lifespan in Caenorhabditis elegans.

Jeremy M Van Raamsdonk, Siegfried Hekimi,

The oxidative stress theory of aging postulates that aging results from the accumulation of molecular damage caused by reactive oxygen species (ROS) generated during normal metabolism. Superoxide dismutases (SODs) counteract this process by detoxifying superoxide. It has previously been shown that elimination of either cytoplasmic or mitochondrial SOD in yeast, ... Read more >>

PLoS Genet (PLoS genetics)
[2009, 5(2):e1000361]

Cited: 245 times

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Huntingtin inhibits caspase-3 activation.

Yu Zhang, Blair R Leavitt, Jeremy M van Raamsdonk, Ioannis Dragatsis, Dan Goldowitz, Marcy E MacDonald, Michael R Hayden, Robert M Friedlander,

Huntington's disease results from a mutation in the HD gene encoding for the protein huntingtin. The function of huntingtin, although beginning to be elucidated, remains largely unclear. To probe the prosurvival function of huntingtin, we modulate levels of wild-type huntingtin in a number of cellular and in vivo models. Huntingtin ... Read more >>

EMBO J. (The EMBO journal)
[2006, 25(24):5896-5906]

Cited: 48 times

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Testicular degeneration in Huntington disease.

Jeremy M Van Raamsdonk, Zoe Murphy, David M Selva, Reza Hamidizadeh, Jacqueline Pearson, Asa Petersén, Maria Björkqvist, Cameron Muir, Ian R Mackenzie, Geoffrey L Hammond, A Wayne Vogl, Michael R Hayden, Blair R Leavitt,

Huntington disease (HD) is an adult onset, neurodegenerative disorder that results from CAG expansion in the HD gene. Recent work has demonstrated testicular degeneration in mouse models of HD and alterations in the hypothalamic-pituitary-gonadal (HPG) axis in HD patients. Here, we show that HD patients have specific testicular pathology with ... Read more >>

Neurobiol. Dis. (Neurobiology of disease)
[2007, 26(3):512-520]

Cited: 45 times

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Phenotypic abnormalities in the YAC128 mouse model of Huntington disease are penetrant on multiple genetic backgrounds and modulated by strain.

Jeremy M Van Raamsdonk, Martina Metzler, Elizabeth Slow, Jacqueline Pearson, Claudia Schwab, Jeffrey Carroll, Rona K Graham, Blair R Leavitt, Michael R Hayden,

The YAC128 mouse model of Huntington disease (HD) exhibits motor abnormalities, cognitive dysfunction and selective neuropathology which are similar to the human disease. Backcrossing YAC128 mice from the FVB/N strain onto the C57BL/6 strain and the 129 strain revealed that striatal volume loss and motor dysfunction are penetrant on all ... Read more >>

Neurobiol. Dis. (Neurobiology of disease)
[2007, 26(1):189-200]

Cited: 50 times

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Wild-type huntingtin ameliorates striatal neuronal atrophy but does not prevent other abnormalities in the YAC128 mouse model of Huntington disease.

Jeremy M Van Raamsdonk, Jacqueline Pearson, Zoe Murphy, Michael R Hayden, Blair R Leavitt,

Huntington disease (HD) is an adult onset neurodegenerative disorder caused by a polyglutamine expansion in the huntingtin (htt) protein. Htt function is essential for embryonic survival as well as normal function during the postnatal period. In addition to having roles in transcription and transport, recent evidence demonstrates that wild-type htt ... Read more >>

BMC Neurosci (BMC neuroscience)
[2006, 7:80]

Cited: 31 times

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Selective degeneration in YAC mouse models of Huntington disease.

Jeremy M Van Raamsdonk, Simon C Warby, Michael R Hayden,

Huntington disease (HD) is one of at least nine polyglutamine disorders caused by a CAG expansion in the coding region of a disease-causing gene. These disorders are characterized by selective degeneration of different regions of the brain, which is not explained by the expression pattern of the mutant protein. In ... Read more >>

Brain Res. Bull. (Brain research bulletin)
[2007, 72(2-3):124-131]

Cited: 23 times

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Cystamine treatment is neuroprotective in the YAC128 mouse model of Huntington disease.

Jeremy M Van Raamsdonk, Jacqueline Pearson, Craig D C Bailey, Daniel A Rogers, Gail V W Johnson, Michael R Hayden, Blair R Leavitt,

Huntington disease (HD) is an adult onset neurodegenerative disorder characterized by selective atrophy and cell loss within the striatum. There is currently no treatment that can prevent the striatal neuropathology. Transglutaminase (TG) activity is increased in HD patients, is associated with cell death, and has been suggested to contribute to ... Read more >>

J. Neurochem. (Journal of neurochemistry)
[2005, 95(1):210-220]

Cited: 60 times

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Body weight is modulated by levels of full-length huntingtin.

Jeremy M Van Raamsdonk, William T Gibson, Jacqueline Pearson, Zoe Murphy, Ge Lu, Blair R Leavitt, Michael R Hayden,

Huntington disease is an adult-onset neurodegenerative disorder that is caused by the expansion of a polyglutamine tract within the Huntingtin (htt) protein. Wild-type htt has been shown to be involved in transcription, transport and cell survival. Here, we demonstrate that increased expression of full-length wild-type htt in mice is associated ... Read more >>

Hum. Mol. Genet. (Human molecular genetics)
[2006, 15(9):1513-1523]

Cited: 57 times

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