Featured Research

from universities, journals, and other organizations

New mechanism links cellular stress and brain damage

Date:
December 13, 2010
Source:
Cell Press
Summary:
A new study uncovers a mechanism linking a specific type of cellular stress with brain damage similar to that associated with neurodegenerative disease. The research is the first to highlight the significance of the reduction of a specific calcium signal that is directly tied to cell fate.

A new study uncovers a mechanism linking a specific type of cellular stress with brain damage similar to that associated with neurodegenerative disease. The research, published by Cell Press in the Dec. 9 issue of the journal Neuron, is the first to highlight the significance of the reduction of a specific calcium signal that is directly tied to cell fate.

Body cells are constantly exposed to various environmental stresses. Although cells possess some natural defenses, excessive stress can lead to a type of cell death called apoptosis. "It is thought that excessive stress impacts brain function by inducing neuronal apoptosis and may play a role in neurodegenerative diseases such as Alzheimer's disease and Huntington's disease (HD)," explains senior study author, Dr. Katsuhiko Mikoshiba, from the Laboratory for Developmental Neurobiology at RIKEN Brain Science Institute.

HD is also associated with abnormal calcium signaling and the accumulation of misfolded proteins. Altered function of an intracellular structure called the endoplasmic reticulum (ER) that plays a key role in protein "quality control" and is a critical regulator of intracellular calcium signaling has been implicated in HD pathogenesis, but the specific underlying mechanisms linking ER stress with calcium and apoptosis are poorly understood.

Dr. Mikoshiba and colleagues demonstrated that a neuronal protein called inositol 1,4,5-trisphosphate receptor 1 (IP3R1) which regulates cellular calcium signaling was destroyed by ER stress and subsequently induced neuronal cell death and brain damage. The researchers went on to show that a protective "chaperone" protein called GRP78 positively regulated IP3R1 and that ER stress led to an impaired IP3R1-GRP78 interaction, which has also been observed in an animal model of HD.

"Based on our observation that the functional interaction between IP3R1 and GRP78 is impaired during ER stress and in the HD model, we propose that IP3R1 functions to protect the brain against stress and that the linkage between ER stress, IP3/calcium signaling, and neuronal cell death are associated with neurodegenerative disease." concludes Dr. Mikoshiba.


Story Source:

The above story is based on materials provided by Cell Press. Note: Materials may be edited for content and length.


Journal Reference:

  1. Takayasu Higo, Kozo Hamada, Chihiro Hisatsune, Nobuyuki Nukina, Tsutomu Hashikawa, Mitsuharu Hattori, Takeshi Nakamura, Katsuhiko Mikoshiba. Mechanism of ER Stress-Induced Brain Damage by IP3 Receptor p865. Neuron, 2010; 68 (5): 865-878 DOI: 10.1016/j.neuron.2010.11.010

Cite This Page:

Cell Press. "New mechanism links cellular stress and brain damage." ScienceDaily. ScienceDaily, 13 December 2010. <www.sciencedaily.com/releases/2010/12/101208125620.htm>.
Cell Press. (2010, December 13). New mechanism links cellular stress and brain damage. ScienceDaily. Retrieved April 23, 2014 from www.sciencedaily.com/releases/2010/12/101208125620.htm
Cell Press. "New mechanism links cellular stress and brain damage." ScienceDaily. www.sciencedaily.com/releases/2010/12/101208125620.htm (accessed April 23, 2014).

Share This



More Health & Medicine News

Wednesday, April 23, 2014

Featured Research

from universities, journals, and other organizations


Featured Videos

from AP, Reuters, AFP, and other news services

Big Pharma Braces for M&A Wave

Big Pharma Braces for M&A Wave

Reuters - Business Video Online (Apr. 22, 2014) Big pharma on the move as Novartis boss, Joe Jimenez, tells Reuters about plans to transform his company via an asset exchange with GSK, and Astra Zeneca shares surge on speculation that Pfizer is looking for a takeover. Joanna Partridge reports. Video provided by Reuters
Powered by NewsLook.com
Study Says Most Crime Not Linked To Mental Illness

Study Says Most Crime Not Linked To Mental Illness

Newsy (Apr. 22, 2014) A new study finds most crimes committed by people with mental illness are not caused by symptoms of their illness or disorder. Video provided by Newsy
Powered by NewsLook.com
Hagel Gets Preview of New High-Tech Projects

Hagel Gets Preview of New High-Tech Projects

AP (Apr. 22, 2014) Defense Secretary Chuck Hagel is given hands-on demonstrations Tuesday of some of the newest research from DARPA _ the military's Defense Advanced Research Projects Agency program. (April 22) Video provided by AP
Powered by NewsLook.com
How Smaller Plates And Cutlery Could Make You Feel Fuller

How Smaller Plates And Cutlery Could Make You Feel Fuller

Newsy (Apr. 22, 2014) NBC's "Today" conducted an experiment to see if changing the size of plates and utensils affects the amount individuals eat. Video provided by Newsy
Powered by NewsLook.com

Search ScienceDaily

Number of stories in archives: 140,361

Find with keyword(s):
Enter a keyword or phrase to search ScienceDaily for related topics and research stories.

Save/Print:
Share:

Breaking News:
from the past week

In Other News

... from NewsDaily.com

Science News

Health News

Environment News

Technology News



Save/Print:
Share:

Free Subscriptions


Get the latest science news with ScienceDaily's free email newsletters, updated daily and weekly. Or view hourly updated newsfeeds in your RSS reader:

Get Social & Mobile


Keep up to date with the latest news from ScienceDaily via social networks and mobile apps:

Have Feedback?


Tell us what you think of ScienceDaily -- we welcome both positive and negative comments. Have any problems using the site? Questions?
Mobile: iPhone Android Web
Follow: Facebook Twitter Google+
Subscribe: RSS Feeds Email Newsletters
Latest Headlines Health & Medicine Mind & Brain Space & Time Matter & Energy Computers & Math Plants & Animals Earth & Climate Fossils & Ruins