Public Release: 

JCI early table of contents for July 25, 2013

JCI Journals

A lifespan-extending drug has limited effects on aging

The immunosuppressive drug rapamycin has been shown to increase longevity in mice even when treatment begins at an advanced age. It is unclear if the extension of life also correlates with prolonged health and vigor. In the current issue of the Journal of Clinical Investigation, Dan Ehninger and colleagues at the German Center for Neurodegenrative Diseases evaluated age-associated characteristics in mice treated with rapamycin. They found that rapamycin improved memory and spatial learning, reduced thyroid follicle size, and reduced body fat in older mice. However, many of these same attributes were also improved in young mice treated with the drug, indicating an age-independent drug effect. The prevalence of cancer, a common cause of mouse mortality, was also decreased in older treated mice. The authors did find that rapamycin treatment had no effect on several age related symptoms, including cardiovascular and liver function, loss of muscle mass, strength retention, or balance. These data suggest that rapamycin treatment may increase lifespan through reduction of cancer rates, and the drug may be useful for relief of some age related conditions. In the accompanying commentary, Arlan Richards of the University of Texas Health Science Center at San Antonio suggests that clinical trials to study the effect of rapamycin on age related neurodegenerative diseases of the elderly such as Alzheimer's disease should be considered.

TITLE: Rapamycin extends murine lifespan but has limited effects on aging

Dan Ehninger
German Center for Neurodegenerative Diseases (DZNE), Bonn, UNK, DEU
Phone: +4922844302530; Fax: +4922844302689; E-mail:

View this article at:


TITLE: Rapamycin, anti-aging, and avoiding the fate of Tithonus

Arlan Richardson
University of Texas Health Sciences Center at San Antonio, San Antonio, TX, USA
Phone: 210-567-3800; E-mail:

View this article at:

A molecular chaperon prevents antibiotic associated hearing loss

An underlying cause of hearing loss is the death of sensory hair cells in the inner ear, which can be damaged in response to a variety of factors including the use of aminoglycoside antibiotics. Previous research has shown that sensory hair cell death in response to antibiotic treatment can be prevented by triggering the expression of HSP70, a member of the heat shock family of proteins that are induced by cellular stress. In this issue of the Journal of Clinical Investigation, Lisa Cunningham and colleagues at the National Institutes of Health investigate the mechanism underlying the protective effect of HSP70 on antibiotic induced hair cell loss. This group found that HSP70 is produced and secreted by the supporting cells of the inner ear in response to heat shock. Extracellular HSP70 produced either by supporting cells or added exogenously prevented antibiotic induced hair cell death. In the companion commentary Rona Giffard and colleagues at the Stanford University School of Medicine point out that there are no current treatments for prevention of aminoglycoside induced hearing loss and that extracellular HSP70 has potential to be used therapeutically.

TITLE: Inner Ear Supporting Cells Protect Hair Cells by Secreting HSP70

Lisa L. Cunningham
NIH/NIDCD, Rockville, MD, USA
Phone: 3014432766; E-mail:

View this article at:


TITLE: The future of molecular chaperones and beyond

Rona Giffard
Stanford School of Medicine, Stanford, CA, USA
Phone: 650-725-8482; Fax: 650 725 8052; E-mail:

View this article at:

Adenosine therapy reduces seizures and progression of epilepsy

Epilepsy is characterized by recurrent seizures that present in many different ways. In some cases epileptic patients exhibit a progressive increase in both frequency and severity of seizures. Epigenetic changes such as DNA methylation have recently been implied as an underlying cause of several neurologic disorders, including epilepsy. In this issue of the Journal of Clinical Investigation, Detlev Boison and colleagues at Legacy Research show an increase of DNA methylation in the hippocampi of epileptic animals. They found that increased methyation corresponded with a decrease of adenosine (ADO), which is a known anticonvulsant. The authors used bioengineered implants to transiently deliver ADO to the brains of epileptic rats. Targeted ADO delivery to the brain reversed DNA hypermethylation and resulted in a decrease in seizures and prevented epilepsy progression. These data indicate that therapies aimed at reducing DNA methylation in the brain have potential for the treatment and prevention of epilepsy.

TITLE: Epigenetic changes induced by adenosine augmentation therapy prevent epileptogenesis

Detlev Boison
Legacy Research, Portland, OR, USA
Phone: (503) 413-1754; Fax: (503) 413-5465; E-mail:

View this article at:


TITLE: Egr1 directs tendon differentiation and promotes tendon repair

Delphine Duprez
CNRS, Paris, , FRA
Phone: + 33 (0)1 44 27 27 53; E-mail:

View this article at:

TITLE: The nucleotide sugar UDP-glucose mobilizes long-term repopulating primitive hematopoietic cells

Byeong Chel Lee
University of Pittsburgh Cancer Institute, Pittsburgh, PA, USA
Phone: 412-623-2285; E-mail:

View this article at:

TITLE: Somitic disruption of GNAS in chick embryos mimics progressive osseous heteroplasia

Li Zeng
Tufts University, Boston, MA, USA
Phone: 617-636-2107; E-mail:

View this article at:

TITLE: Isocitrate ameliorates anemia by suppressing the erythroid iron restriction response

Adam Goldfarb
University of Virginia, Charlottesville, VA, USA
Phone: 434-982-0593; Fax: 434-924-1545; E-mail:

View this article at:

TITLE: CHIP protects against cardiac pressure overload through regulation of AMPK

Cam Patterson
University of North Carolina at Chapel Hill, Chapel Hill, NC, USA
Phone: 919-843-6477; Fax: 9198434585; E-mail:

View this article at:

TITLE: Immunoglobulin-like domain containing receptor 1 mediates fat-stimulated cholecystokinin secretion

Rodger A. Liddle
Duke University Medical Center, Durham, NC, USA
Phone: 919 681-6380; E-mail:

View this article at:


Disclaimer: AAAS and EurekAlert! are not responsible for the accuracy of news releases posted to EurekAlert! by contributing institutions or for the use of any information through the EurekAlert system.