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Claudio Torres

Claudio Torres, PhD

Research Associate Professor


Department: Pathology & Laboratory Medicine

Education

  • PhD in Molecular and Cell Biology - University of Concepcion, Chile

Memberships / Professional Affiliations

Memberships, Professional Affiliations and Editorial Positions

  • American Society for Cell Biology
  • American Aging Association
  • Gerontological Society of America
  • GRS/IGF Society
  • American Society for Investigative Pathology (ASIP)
  • American Society for Investigative Pathology
  • Society for Free Radical Biology and Medicine
  • Associate Editor, Endocrinology of Aging, Frontiers in Endocrinology
  • Grant Review, Special Emphasis NeuroAIDS, NIH
  • Grant Review. Special Emphasis/The Brain Disorders and Clinical Neuroscience (BDCN), NIH
  • Grant Review, Alzheimer's Association
  • Reviewer, Journals: Molecular and Cellular Neuroscience, Journal of Neuroscience, Trends in Neurosciences, Brain Research, Free Radical Research, Journal of Biological Chemistry, Journal of Gerontology, Aging Cell

Dr. Torres is a research associate professor in the Department of Pathology and Laboratory Medicine at Drexel University College of Medicine. He also serves as director of the medical biochemistry course in his role as adjunct faculty at Jefferson College of Graduate Studies.

Dr. Torres has served as a mentor to undergraduate and graduate students doing research on aging, particularly in the field of astrocyte senescence.

Research Interests

Mechanisms of aging that predispose to neurocognitive disease. Cellular senescence in human brain during aging and neuropathology; role of senescent cells in inflammatory response in Alzheimer's disease and HIV-associated neurocognitive disorders; use of markers of senescence for early detection of Alzheimer's disease.

Research

Aging is the greatest risk factor for the development of most of neurodegenerative disorders; however, the aspects of the aging process that predispose us to the development of brain pathology are largely unknown. My laboratory is a pioneer in studying the role of cellular senescence on brain physiology during normal aging and neuropathology. The senescence process is an irreversible growth arrest triggered by various events including telomere dysfunction, DNA damage, oncogene activation, oxidative stress and proteasome inhibition. The presence of senescent cells in the human brain could be critical because they display an altered pattern of secretion known as the senescence-associated secretory phenotype (SASP), a complex mixture of factors that profoundly affect neighboring cells and tissues by creating a pro-inflammatory microenvironment.

While neurons are the major target of neuropathology, neuronal function depends on the activity of supporting cells including astrocytes and microglia. Our studies indicate that human astrocytes activate the senescence program in response to oxidative stress, exhaustive replication and beta amyloid, and we have demonstrated that in the human brain the number of senescent astrocytes increases with age, and remarkably, more so in patients suffering from Alzheimer's disease. We have evidence that astrocyte senescence is also accompanied by profound changes in their transcriptome, including the loss of brain-specific transcripts, which suggests the loss of differentiated function in senescent astrocytes. In addition to our studies in Alzheimer's patients, we have evidence indicating that markers of senescence can also be detected in glia and cortical neurons of patients suffering from frontotemporal lobar degeneration (FTLD) and HIV-1 infection. The pathogenic mechanisms involved in the origin and progression of these neurodegenerative diseases are still unclear but they have overlapping biomarkers, and we propose cellular senescence as a common underling mechanism.

The demonstration that senescent cells accumulate in the brain during aging and pathology, and that these cells lose functionality, enhances our understanding of why age is the major risk factor for neurodegenerative diseases, and may lead the way to interventions aimed at delaying senescence or reducing the effects of senescent cells in the progression of neurodegenerative diseases.

Our current research efforts include:

  1. Verifying the extension of senescence to other cells types, and brain areas affected by AD, FTLD, and HIV-associated neurodegenerative disease by analyzing functional markers of senescence including chromatin condensation, telomere dysfunction, and epigenetic changes in histones.
  2. Evaluation of the relationship between brain metabolism, oxidative stress and senescence.
  3. Studies to evaluate the role of HIV-infection, HIV surface protein gp120, highly active antiretroviral therapy (HAART), and drugs of abuse, cocaine and morphine, as inducers of the senescence program on astrocytes and microglia.
  4. Determining the role of exosomal miRNAs secreted by senescent astrocytes as biosensors for early detection of Alzheimer's disease.
  5. Evaluating the ability of senescent astrocytes to influence microglial activation and neuronal senescence.
  6. Characterizing mechanisms involved in SASP regulation in astrocytes and microglia, and its role as a contributor to brain inflammation.
  7. Evaluation of the role of senescence in astrocytes' handling of Aβ.
  8. Assess the capacity of rapamycin to modulate senescence in vitro and in AD mouse models.

In the Media

"The Age Factor"
Exel - Drexel University Research Magazine (2013)

"Ageing cells offer new target for Alzheimer’s therapy"
New Scientist (September 26, 2012)

Alzheimer's May Be Result of Natural Anti-Cancer Mechanism
MediLexicon (October 4, 2012)

"Considering Senescent Astrocytes in Alzheimer's Disease"
Fight Aging (September 20, 2012)

Publications

"lmplications of Cellular Senescence on Aging and Disease in the Brain"
Crowe E, Tuzer F, Cohen J, Yetkin E, D'Agostino L, Sell C and Torres C
Springer Publishers, Healthy Ageing and Longevity, (series editors: Leonard Hayflick and Suresh Rattan) in press, 2015

"Senescence Associated Secretory Phenotype profile from primary Iung mice fibroblasts depends on the senescence induction stimuli"
Maciel-Barón LA, Morales-Rosales SL, Aquino-Cruz AA, Triana-Martínez F, Sonia Galván-Arzate, Luna-López A, González-Puertos VY, López-Díazguerrero NE, Torres C, Königsberg M
AGE 2015, in press.

"Mitochondrial Reactive Oxygen Species in Cellular Senescence"
Nacarelli T, Torres C, Sell
Springer Publishers, Healthy Ageing and Longevity (series-editors: Leonard Hayflick and Suresh Rattan) in press, 2015

"Detecting senescence: methods and approaches"
Crowe EP, Nacarelli T, Bitto A, Lerner C, Sell C, Torres C
Methods Mol Biol; 1170:425-45, 2014

"The senescence arrest program and the cell cycle"
Bitto A, Crowe EP, Lerner C, Torres C, Sell C
Methods Mol Biol; 1170:145-54, 2014

"p62/SQSTM1 at the interface of aging, autophagy, and disease"
Bitto A, Lerner CA, Nacarelli T, Crowe E, Torres C, Sell C
Age (Dordr); 36(3):9626. doi: 10.10071s11357-014-9626-3, ). June 2014

"Mice producing reduced levels of insulin-like growth factor type 1 display an increase in maximum, but not mean, Iife span"
Lorenzini A, Salmon AB, Lerner C, Torres C, Ikeno Y, Motch S, McCarter R, Sell C
J Gerontol A Biol Sci Med Sci;69(4):410-9, Apr 2014

"Reduced mammalian target of rapamycin activity facilitates mitochondrial retrograde signaling and increases life span in normal human fibroblasts"
Lerner C, Bitto A, Pulliam D, Nacarelli T, Konigsberg M, Van Remmen H, Torres C, Sell C
Aging Cell; 12(6):966-77, Dec 2013

"Astrocyte Senescence as a Component of Alzheimer's Disease"
Bhat R, Crowe E, Moh M, Bitto A, Katsetos C, Garcia F, Johnson B, Trojanowsky J, Sell C, and Torres C
PLoS One; 7(9):e45069, 2012

"Relationship of spindle assembly checkpoint fidelity to species body mass, lifespan, and developmental rate"
Lorenzini A, Fink L, Stamato T, Torres C, Sell C
Aging (impact journal series) Vol.3 No.12 pp.1206-1212, Dec 2011

"Stress-induced senescence in human and rodent astrocytes"
Bitto A, Sell C, Crowe E, Lorenzini A, Malaguti M, Hrelia S, Torres C
Exp Cell Res., 316(17):2961-8, 2010

"Long-term IGF-I exposure decreases autophagy and cell viability"
Bitto A, Lerner C, Torres C, Roell M, Malaguti M, Perez V, Lorenzlni A, Hrelia S, lkeno Y, Matzko ME, McCarter R, Sell C
PLoS One; 5(9):e12592, Sep 7, 2010

"Activation of proteasome by IGF-I may enhance clearance of oxidized proteins in the brain"
Crowe E, Sell C, Jeff D, Thomas J, Johannes G, Torres C
Mech. Aging Dev, 130: 793-800, 2009

"The release of sympathetic neurotransmitters is impaired in aged rats after an inflammatory stimulus: a possible link between cytokine production and sympathetic transmission"
Donoso V, Gomez CR, Orriantia MA, Pérez V, Torres C, Coddou C, Nelson P, Maisey K, Morales B, Fernandez R, Imarai M, Huidobro-Toro JP, Sierra F, Acuña-Castillo C
Mech Ageing Dev.; 129(12):728-34, Dec 2008

"Discovery of a human peptide sequence signaling islet neogenesis"
Levetan CS, Upham LV, Deng S, Laury-Kleintop L, Kery V, Nolan R, Quinlan J, Torres C, El-Hajj RJ.
Endocr Pract; 14(9):1075-83, Dec 2008

"Proteasome modulates mitochondrial function during the senescence of human fibroblasts"
Torres C and Perez V
Free Radic Biol Med. 44, 403-14, 2008

"Modulation of replicative senescence of diploid human cells by nuclear ERK signaling"
Tresini M, Lorenzini A, Torres C, Cristofalo VJ
J Biol Chem.; 282(6):4136-51, Feb 9, 2007

"Proteasome Inhibitors Shorten Replicative Life Span and Induce a Senescent-like Phenotype of Human Fibroblasts"
Torres C, Lewis L, Cristofalo VJ
J Cell Physiol; 207(3):845-53, Jun 2006

"T-kininogen: a biomarker of aging in Fisher 344 rats with possible implications on the immune response"
Acuña C, Leiva E, Gómez C, Pérez V, Li M, Torres C, Walter R, Murasko D, Sierra F
J Gerontol A Biol Sci Med Sci;61(7):641-9, Jul 2006

"Serum from aged F344 rats conditions the activation of young macrophages"
Gómez C, Acuña C, Nishimura S, Pérez V, Escobar A, Sabaj V, Torres C, Walter R, Sierra F
Mech Ageing Dev.;127(3).257-63, Mar 2006

"Replicative senescence: a critical review
Cristofalo VJ, Lorenzini A, Allen RG, Torres C, Tresini M.
Mech Ageing Dev; 125(10-11):827-48, Oct-Nov 2004

"Metabolic Stabilization of MKP2 in Wl38 Human Senescent Fibroblasts"
Torres C, Francis MK, Lorenzini A, Tresini M, Cristofalo V.
J. Exp Cell Res; 290(2):195-206, Nov 1, 2003


Contact Information


Academic Office

Department of Pathology & Laboratory Medicine
245 N. 15th Street
MS 435
Philadelphia, PA 19102
Phone: 215.762.1783
Fax: 215.762.3978