527 results match your criteria Science of aging knowledge environment : SAGE KE[Journal]


I come not to bury SAGE KE but to appraise It.

Authors:
Evelyn Strauss

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):vp1. Epub 2006 Jun 28.

This article serves as a eulogy for the Science of Aging Knowledge Environment (SAGE KE). This online resource--Science's Web site on aging--is publishing its last issue today. The piece is a personal recollection of co-creating the site--and includes some thoughts on how the field of aging has changed over the last six years. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.vp1DOI Listing
June 2006
3 Reads

Targeting the role of the endosome in the pathophysiology of Alzheimer's disease: a strategy for treatment.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):re2. Epub 2006 Jun 28.

CNS Discovery, Global Research & Development, Pfizer Inc., Groton, CT 06234, USA.

Membrane-bound endosomal vesicles play an integral role in multiple cellular events, including protein processing and turnover, and often critically regulate the cell-surface availability of receptors and other plasma membrane proteins in many different cell types. Neurons are no exception, being dependent on endosomal function for housekeeping and synaptic events. Growing evidence suggests a link between neuronal endosomal function and Alzheimer's disease (AD) pathophysiology. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.re2DOI Listing
June 2006
1 Read

From bedside to bench: does mental and physical activity promote cognitive vitality in late life?

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe21. Epub 2006 Jun 28.

School of Medicine and VA Pittsburgh GRECC, University of Pittsburgh, Pittsburgh, PA 15213, USA.

A wide range of animal and human studies provide evidence for the potential of physical and cognitive exercise in promoting cognitive health later in life. The effects of such activities on intermediate outcomes, such as cognitive performance, are becoming clearer, as are the molecular mechanisms involved. Physical and cognitive exercise might increase "cognitive reserve" and increase the overall health of the brain, thereby reducing or delaying cognitive impairment and dementia. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.pe21DOI Listing
June 2006
1 Read

The unusual genetics of human longevity.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe20. Epub 2006 Jun 28.

Department of Cell Biology, University of Calabria, Calabria, Italy.

In no species other than humans do cultural, social, and biological factors interact with each other in modulating complex phenotypes. Thus, the identification of genetic factors that affect human longevity is a true challenge. The model of centenarians provides us a unique opportunity to tackle this challenge. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.pe20DOI Listing
June 2006
8 Reads

A work in progress: the metabolic syndrome.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe19. Epub 2006 Jun 28.

Taub Institute for Research of Alzheimer's Disease and the Aging Brain, Columbia University, New York, NY, USA.

Metabolic syndrome refers to a constellation of risk factors for cardiovascular disease. They include elevated plasma glucose concentrations, dyslipidemia, hypertension, and abdominal obesity. These conditions typically occur during middle age or later in life. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.pe19DOI Listing
June 2006
3 Reads

WRN's tenth anniversary.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe18. Epub 2006 Jun 28.

Department of Neurology, Yale University, New Haven, CT 06520, USA.

Werner syndrome (WS) is a segmental progeroid syndrome in which patients display pleiotropic features of aging seen in the normal population. The advent of positional cloning in the 1990s markedly accelerated the identification of human disease-causing genes. In 1996, mutations in WRN, which was shown to encode a new, putative member of the family of RecQ DNA helicases, were identified in four patients as the cause of WS. Read More

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June 2006
6 Reads

Developing a research agenda in biogerontology: physiological systems.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe17. Epub 2006 Jun 28.

Biology of Aging Program, National Institute on Aging, Bethesda, MD 20892, USA.

The Biology of Aging Program (BAP) at the National Institute on Aging supports research in many areas, including processes of cell senescence and apoptosis, genetic influences on aging, and how aging leads to tissue dysfunction. Several approaches to research on aging physiological systems are described, along with BAP programmatic efforts to enhance and support that research. Understanding the relation between aging and tissue dysfunction has led to new insights into how health can be improved for aged individuals. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.pe17DOI Listing
June 2006
4 Reads

Aging on the job.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe16. Epub 2006 Jun 28.

Mayo Clinic, Rochester, MN 55905, USA.

The older population is growing faster than the population as a whole. Paid work is the main mechanism for physical activity in humans. We, therefore, wanted to ascertain whether work practices (such as employment status and the types of tasks workers perform) follow the biological decline in physical activity that occurs with aging in humans and many other species. Read More

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June 2006
2 Reads

The role of mitochondria in conserved mechanisms of aging.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):pe15. Epub 2006 Jun 28.

Department of Molecular Developmental Biology, Institute of Molecular Biosciences, J. W. Goethe University, Max-von-Laue-Strasse 9, 60438 Frankfurt, Germany.

The European research project MiMage, supported by the European Community's Sixth Framework for Research and Technological Development, focuses on elucidating the role of mitochondria in conserved mechanisms of aging. This Perspective summarizes a selection of talks presented in April 2006 at the second MiMage symposium by members from participating laboratories and invited speakers. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.pe15DOI Listing
June 2006
1 Read

Death-bed prophecy.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):nf17. Epub 2006 Jun 28.

What's left to learn about aging? The burning question for many researchers is whether life-stretching pathways and genes from model organisms boost human life span. Researchers might be able to track down additional genes and pathways that adjust longevity by studying a broader range of organisms or by tracking the evolution of genes that promote aging. An alternative way to extend our lives might be to identify the genes behind late-life killers such as heart disease and diabetes. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.nf17DOI Listing
June 2006
2 Reads

The age of cancer.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):nf16. Epub 2006 Jun 28.

The biggest risk factor for cancer isn't smoking or bad diet or anything a person can avoid. It's growing old. New findings might help explain the connection between aging and cancer. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.nf16DOI Listing
June 2006
3 Reads

Dementia with cerebrovascular disease.

Sci Aging Knowledge Environ 2006 Jun 28;2006(10):dn1. Epub 2006 Jun 28.

Columbia University College of Physicians and Surgeons, Department of Neurology, New York, NY 10032, USA.

In this case study, we review the symptoms, cognitive testing, brain imaging, and brain pathology of a woman with dementia, for whom the neuropathological findings suggest a prominent contribution of cerebrovascular disease. Vascular dementia is the term commonly used for persons with dementia resulting from strokes, either clinically evident or subclinical "silent" events. "Mixed dementia" is the term used when there is an admixture of pathological findings related to Alzheimer's disease (AD) and cerebrovascular disease, as in this situation. Read More

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http://dx.doi.org/10.1126/sageke.2006.10.dn1DOI Listing
June 2006
2 Reads
1 Citation

Aging at the interface of stem cell renewal, apoptosis, senescence, and cancer.

Sci Aging Knowledge Environ 2006 May 24;2006(9):pe14. Epub 2006 May 24.

Institute of Clinical Molecular Biology, University of Kiel, Germany.

The aging-related research field has focused on the detection of genetic factors that affect the aging process, but more recently scientists have started to shift their attention to novel and more integrative ways of studying cellular and organismal function. Such approaches allow them to uncover and explore unexpected patterns and themes, resulting in a more comprehensive knowledge of the complex regulatory pathways and networks involved in aging and age-related diseases. Eventually, this knowledge will lead to a systems-level understanding of aging. Read More

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http://dx.doi.org/10.1126/sageke.2006.9.pe14DOI Listing
May 2006
1 Read

The age of skin cancers.

Sci Aging Knowledge Environ 2006 May 24;2006(9):pe13. Epub 2006 May 24.

Department of Dermatology, Baylor College of Medicine, Houston, TX 77030, USA.

Cancer affects two major cell types in the human skin: epithelial cells and melanocytes. Aging and a previous history of ultraviolet light exposure are major risk factors for skin cancers, including basal and squamous cell carcinomas and melanomas. However, melanomas, which are the most deadly of the skin tumors, display two intriguing characteristics: The incidence is increased and the prognosis is worse in males over 60 years as compared with females of the same age. Read More

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http://dx.doi.org/10.1126/sageke.2006.9.pe13DOI Listing
May 2006
1 Read

Stem cell aging and cancer.

Authors:
Jennifer Fuller

Sci Aging Knowledge Environ 2006 May 24;2006(9):pe12. Epub 2006 May 24.

Immunology Program at the University of Michigan, Ann Arbor, MI 48109, USA.

Stem cells are capable of self-renewal, differentiation into various lineages, and proliferation; thus, they play critical roles in the functioning and maintenance of many biological systems. However, these unique qualities of stem cells also make them more vulnerable to mutations as the organism ages. The biggest risk factor in cancer development is age, and most scientists believe that cancers partly result from a buildup of mutations in different cell types over time. Read More

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http://dx.doi.org/10.1126/sageke.2006.9.pe12DOI Listing
May 2006
2 Reads

Shortcut to death.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 May 24;2006(9):nf15. Epub 2006 May 24.

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http://dx.doi.org/10.1126/sageke.2006.9.nf15DOI Listing
May 2006
7 Reads

Pushing the envelope.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 May 24;2006(9):nf14. Epub 2006 May 24.

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May 2006
6 Reads

Toward a better understanding of Klotho.

Sci Aging Knowledge Environ 2006 May 3;2006(8):pe11. Epub 2006 May 3.

Department of Pathology and Tumor Biology, Kyoto University Graduate School of Medicine, Kyoto 606-8501, Japan.

klotho mutant mice were originally described as a short-lived mouse model with premature aging-like disorders. The klotho gene responsible for these phenotypes encodes a type I membrane protein with a considerable similarity to beta-glycosidase. klotho is predominantly expressed in tissues functioning in the regulation of calcium homeostasis. Read More

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http://dx.doi.org/10.1126/sageke.2006.8.pe11DOI Listing
May 2006
28 Reads

Neuropathology in Alzheimer's disease: awaking from a hundred-year-old dream.

Sci Aging Knowledge Environ 2006 May 3;2006(8):pe10. Epub 2006 May 3.

Department of Psychiatry and Neurology, Asahikawa Medical College, Asahikawa 078-8510, Japan.

For one hundred years after Alois Alzheimer's first report of Alzheimer's disease (AD) in 1906, the pathological hallmarks of the disease, senile plaques and neurofibrillary tangles (NFTs), have been attractive targets for researchers. Therefore, not surprisingly, efforts to understand disease mechanisms have concentrated on the cell biology of amyloid-beta (Abeta) deposition as senile plaques or on the phosphorylation and aggregation of tau as NFTs. However, it now appears that this focus on pathology as a central contributor to disease may be misguided. Read More

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http://dx.doi.org/10.1126/sageke.2006.8.pe10DOI Listing
May 2006
6 Reads

A shared splice site?

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 May 3;2006(8):nf13. Epub 2006 May 3.

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http://dx.doi.org/10.1126/sageke.2006.8.nf13DOI Listing
May 2006
2 Reads

What good is growing old?

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 May 3;2006(8):nf12. Epub 2006 May 3.

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http://dx.doi.org/10.1126/sageke.2006.8.nf12DOI Listing
May 2006
2 Reads

In praise of insulin resistance.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 May 3;2006(8):nf11. Epub 2006 May 3.

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May 2006
3 Reads

Aging in check.

Sci Aging Knowledge Environ 2006 Apr 5;2006(7):pe9. Epub 2006 Apr 5.

Division of Molecular Carcinogenesis, Department of Medicine, New York Medical College, Valhalla, NY 10595, USA.

The spindle checkpoint monitors the interaction between spindle microtubules and kinetochores to prevent precocious entry into anaphase, delaying this stage of mitosis until all condensed chromosomes have been attached to the mitotic spindle in a bi-oriented manner (so that the two kinetochores associated with a pair of sister chromatids are oriented toward opposite poles of the spindle). In addition to conserved Bub and Mad family members, which are known to function in the spindle checkpoint pathway in organisms ranging from yeast to mammals, two mRNA transport genes, Rae1 and Nup9, are also involved in the spindle checkpoint function in mammals. Biochemically, activated spindle checkpoint components have been shown to suppress the activity of the anaphase promoting complex/cyclosome. Read More

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April 2006
5 Reads

SENS and the polarization of aging-related research.

Sci Aging Knowledge Environ 2006 Apr 5;2006(7):pe8. Epub 2006 Apr 5.

Ottawa Health Research Institute, Ottawa K1H 8L6, Canada.

The second Strategies for Engineered Negligible Senescence conference (SENS II) featured some very provocative ideas. The explicit objective of extending human life span indefinitely has opened a large rift between the meeting's organizer and those who believe he is acting unscientifically, perhaps recklessly. Two SENS conference participants present their views on the divisive nature of SENS. Read More

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http://dx.doi.org/10.1126/sageke.2006.7.pe8DOI Listing
April 2006
3 Reads

Environmental movement.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Apr 5;2006(7):nf9. Epub 2006 Apr 5.

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April 2006
3 Reads

Tag-team recycling.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Apr 5;2006(7):nf10. Epub 2006 Apr 5.

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http://dx.doi.org/10.1126/sageke.2006.7.nf10DOI Listing
April 2006
3 Reads

The development of amyloid beta protein deposits in the aged brain.

Sci Aging Knowledge Environ 2006 Mar 8;2006(6):re1. Epub 2006 Mar 8.

Department of Neuropathology, University of Bonn, D-53105 Bonn, Germany.

The deposition of amyloid beta protein (Abeta) in the human brain and the generation of neurofibrillary tangles are the histopathological hallmarks of Alzheimer's disease. Accumulation of Abeta takes place in senile plaques and in cerebrovascular deposits as a result of an imbalance between Abeta production and clearance. This Review describes the different types of Abeta deposits, which can be distinguished by their morphology and by the hierarchical involvement of distinct areas of the brain in Abeta deposition. Read More

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http://dx.doi.org/10.1126/sageke.2006.6.re1DOI Listing
March 2006
7 Reads

Small-fiber neuropathy: answering the burning questions.

Sci Aging Knowledge Environ 2006 Mar 8;2006(6):pe7. Epub 2006 Mar 8.

Department of Anesthesiology, Neurology, and Neuropathology, Massachusetts General Hospital, Harvard Medical School, Boston, MA 02114, USA.

Small-fiber neuropathy is a peripheral nerve disease that most commonly presents in middle-aged and older people, who develop burning pain in their feet. Although it can be caused by disorders of metabolism such as diabetes, chronic infections (such as with human immunodeficiency virus), genetic abnormalities, toxicity from various drugs, and autoimmune diseases, the cause often remains a mystery because standard electrophysiologic tests for nerve injury do not detect small-fiber function. Inadequate ability to test for and diagnose small-fiber neuropathies has impeded patient care and research, but new tools offer promise. Read More

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http://dx.doi.org/10.1126/sageke.2006.6.pe7DOI Listing
March 2006
6 Reads

Buffing up the family jewels.

Authors:
Mary Beckman

Sci Aging Knowledge Environ 2006 Mar 8;2006(6):nf8. Epub 2006 Mar 8.

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http://dx.doi.org/10.1126/sageke.2006.6.nf8DOI Listing
March 2006
5 Reads

Craving an answer.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Mar 8;2006(6):nf7. Epub 2006 Mar 8.

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March 2006
4 Reads

Olfactory loss in aging.

Authors:
Nancy E Rawson

Sci Aging Knowledge Environ 2006 Feb 8;2006(5):pe6. Epub 2006 Feb 8.

Monell Chemical Senses Center, Philadelphia, PA 19104, USA.

Olfactory loss is a common age-related complaint that may be caused by changes in the anatomy of the structures required for olfaction (for example, loss of olfactory receptor cells) or in the environment surrounding the receptor cell (for example, altered nasal mucus composition). However, aging, as well as age-related diseases and medications, may also alter the distribution, density, or function of specific receptor proteins, ion channels, or signaling molecules that affect the ability of neural elements throughout the olfactory pathway to signal and process odorant information. Although a great deal has been learned about the prevalence and nature of age-related olfactory loss, we are just beginning to explore avenues to prevent or alleviate this sensory deficit. Read More

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February 2006
3 Reads

When good Cdk5 turns bad.

Authors:
Qing Guo

Sci Aging Knowledge Environ 2006 Feb 8;2006(5):pe5. Epub 2006 Feb 8.

Department of Physiology, University of Oklahoma Health Sciences Center, College of Medicine, Oklahoma City, OK 73104, USA.

The cyclin-dependent kinase-5 (Cdk5) is critical to normal mammalian development and has been implicated in synaptic plasticity, learning, and memory in the adult brain. But Cdk-5 activity has also been linked to neurodegenerative diseases. Could a single protein have opposing effects? A new study shows that production of a neuronal protein capable of regulating Cdk-5 activity can turn Cdk-5 from "good" to "bad. Read More

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http://dx.doi.org/10.1126/sageke.2006.5.pe5DOI Listing
February 2006
2 Reads

Mucking with metabolism.

Authors:
Mary Beckman

Sci Aging Knowledge Environ 2006 Feb 8;2006(5):nf6. Epub 2006 Feb 8.

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http://dx.doi.org/10.1126/sageke.2006.5.nf6DOI Listing
February 2006
6 Reads

The sour side of sweet.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Feb 8;2006(5):nf5. Epub 2006 Feb 8.

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February 2006
6 Reads

Prion 2005: Between Fundamentals and Society's Needs.

Authors:
Carina Treiber

Sci Aging Knowledge Environ 2006 Jan 25;2006(4):pe4. Epub 2006 Jan 25.

Freie Universitaet Berlin, Thielallee 63, 14195 Berlin, Germany.

Prion diseases for the most part affect individuals older than 60 years of age and share features with other diseases characterized by protein deposits in the brain, such as Alzheimer's disease and Parkinson's disease. The international conference "Prion 2005: Between Fundamentals and Society's Needs," organized by the German Transmissible Spongiform Encephalopathies Research Platform, aimed to integrate and coordinate the research efforts of participants to better achieve prevention, treatment, control, and management of prion diseases, including Creutzfeldt-Jakob disease and fatal familial insomnia in humans. Several main topics were discussed, such as the molecular characteristics of prion strains, the cell biology of cellular and pathogenic forms of the prion proteins, the pathogenesis of the diseases they cause, emerging problems, and promising approaches for therapy and new diagnostic tools. Read More

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http://dx.doi.org/10.1126/sageke.2006.4.pe4DOI Listing
January 2006
1 Read

The way of the honeybee.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jan 25;2006(4):nf4. Epub 2006 Jan 25.

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January 2006
2 Reads

Dividing to keep muscle together: the role of satellite cells in aging skeletal muscle.

Authors:
Russell T Hepple

Sci Aging Knowledge Environ 2006 Jan 18;2006(3):pe3. Epub 2006 Jan 18.

Faculty of Kinesiology, University of Calgary, Calgary, Alberta, Canada.

The factors responsible for the atrophy of skeletal muscle with aging remain to be elucidated. Recent evidence points toward an important role for a population of cells located on the surface of skeletal muscle fibers, known as satellite cells, in maintaining the integrity of skeletal myocytes throughout the life span. This Perspective examines the role that these cells are thought to play in aging muscle atrophy, and highlights a recent study by Brack and colleagues that attempts to understand the role of satellite cells in maintaining the ratio of myonuclear number to cytoplasmic volume within myocytes as we age. Read More

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http://dx.doi.org/10.1126/sageke.2006.3.pe3DOI Listing
January 2006
1 Read

Double duty.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jan 18;2006(3):nf3. Epub 2006 Jan 18.

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January 2006
2 Reads

Lessons from Drosophila models of DJ-1 deficiency.

Sci Aging Knowledge Environ 2006 Jan 11;2006(2):pe2. Epub 2006 Jan 11.

Institute for Cell Engineering, Department of Neurology, Johns Hopkins University School of Medicine, Baltimore, MD 21205, USA.

Mutations in the DJ-1 gene are associated with rare forms of autosomal recessive early-onset Parkinson's disease (PD). Although the precise physiological function of DJ-1 remains obscure, accumulating evidence suggests that DJ-1 may normally function as a redox-sensitive molecular chaperone that can protect against the deleterious effects of oxidative stress, particularly in mitochondria. Recent studies in the fruit fly, Drosophila melanogaster, have shed further light on the biological role of DJ-1. Read More

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http://dx.doi.org/10.1126/sageke.2006.2.pe2DOI Listing
January 2006
5 Reads

Chain of command.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jan 11;2006(2):nf2. Epub 2006 Jan 11.

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January 2006
5 Reads

Biomarkers of aging: combinatorial or systems model?

Authors:
Andres Kriete

Sci Aging Knowledge Environ 2006 Jan 4;2006(1):pe1. Epub 2006 Jan 4.

School of Biomedical Engineering, Science, and Health Systems, Drexel University, Philadelphia, PA 19104, USA.

Systemwide functional and structural changes caused by the aging process encourage the implementation of new bioinformatics search strategies for markers of aging. Combinatorial biomarkers should be particularly favored, as they can quantify processes on multiple levels of biological organization and overcome an otherwise limited ability to access heterogeneities in populations. An even more challenging but rational approach is the development of systems biology models to describe molecular pathways and key networks mechanistically as they relate to age. Read More

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http://dx.doi.org/10.1126/sageke.2006.1.pe1DOI Listing
January 2006
3 Reads

Uncoupling insulin.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2006 Jan 4;2006(1):nf1. Epub 2006 Jan 4.

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http://dx.doi.org/10.1126/sageke.2006.1.nf1DOI Listing
January 2006
6 Reads

Harnessing hormonal signaling for cardioprotection.

Sci Aging Knowledge Environ 2005 Dec 21;2005(51):re6. Epub 2005 Dec 21.

Department of Medicine, Weill Medical College of Cornell University, New York, NY 10021, USA.

Cardiovascular disease is the leading cause of death in women in the Western world and is predominant among the elderly. A large body of evidence suggests that hormonal signaling plays a critical role in the regulation of cardioprotective mechanisms, as premenopausal women are at significantly lower risk of heart disease compared with men, but the risk greatly increases with the onset of menopause. This association indicates that estrogen may protect the heart from cardiovascular disease. Read More

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http://dx.doi.org/10.1126/sageke.2005.51.re6DOI Listing
December 2005
3 Reads

Loose chromosomes sink cells.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2005 Dec 21;2005(51):nf91. Epub 2005 Dec 21.

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December 2005
5 Reads

When T cells get old.

Authors:
Graham Pawelec

Sci Aging Knowledge Environ 2005 Dec 14;2005(50):pe39. Epub 2005 Dec 14.

Center for Medical Research, University of Tuebingen, D-72072 Tuebingen, Germany.

Why is vaccination against infectious diseases less effective in older patients than in younger ones? Why do the elderly suffer from more frequent and severe infectious episodes than the young? The answer to both these questions is immunosenescence--the poorly defined changes that occur in the immune system as a result of the disrupted performance of multiple components of immunity. Presentations from a recent workshop, which are summarized here, examined these questions and provided some insights from the perspective of improving vaccination strategies among the elderly. Read More

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http://dx.doi.org/10.1126/sageke.2005.50.pe39DOI Listing
December 2005
2 Reads

Oxidants off the hook?

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2005 Dec 14;2005(50):nf90. Epub 2005 Dec 14.

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December 2005
2 Reads

Living Longer and Paying the Price?

Sci Aging Knowledge Environ 2005 Dec 7;2005(49):pe38. Epub 2005 Dec 7.

The Institute on Aging, Department of Pathology and Laboratory Medicine, University of Pennsylvania School of Medicine, Philadelphia, PA 19104, USA.

Over the past century, there have been tremendous increases in longevity in the United States and most other developed countries. If these trends continue, the costs of paying for public programs like Social Security, Medicare, and Medicaid will escalate at a startling rate with the aging of the "baby boomer" generation. A meeting titled "Living Longer and Paying the Price?" was organized to consider whether current trends in longevity will continue at the current pace, accelerate, or decelerate as a result of public health problems such as obesity and infectious diseases. Read More

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http://dx.doi.org/10.1126/sageke.2005.49.pe38DOI Listing
December 2005
5 Reads

Tapping into renewal.

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2005 Dec 7;2005(49):nf89. Epub 2005 Dec 7.

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http://dx.doi.org/10.1126/sageke.2005.49.nf89DOI Listing
December 2005
5 Reads

T Cell Immunity and Aging.

Sci Aging Knowledge Environ 2005 Nov 30;2005(48):pe37. Epub 2005 Nov 30.

Center for Medical Research, University of Tuebingen, D-72072 Tuebingen, Germany.

The effect of age on the immune system is generally detrimental and results in "immunosenescence," a poorly-defined state inadequately reflected in clinical data and for which few reliable "biomarkers of aging" are available. The multinational consortium "T-Cell Immunity in Ageing," T-CIA, was set up to examine these issues specifically as applied to T lymphocytes. This Perspective discusses some of the outcomes of a recent conference that considered progress toward resolving these questions in humans. Read More

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http://dx.doi.org/10.1126/sageke.2005.48.pe37DOI Listing
November 2005
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Down with p53!

Authors:
Mitch Leslie

Sci Aging Knowledge Environ 2005 Nov 30;2005(48):nf88. Epub 2005 Nov 30.

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http://dx.doi.org/10.1126/sageke.2005.48.nf88DOI Listing
November 2005
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