WELCOME TO OUR PARKINSON'S PLACE!

I HAVE PARKINSON'S DISEASES AND THOUGHT IT WOULD BE NICE TO HAVE A PLACE WHERE THE CONTENTS OF UPDATED NEWS IS FOUND IN ONE PLACE. THAT IS WHY I BEGAN THIS BLOG.

I COPY NEWS ARTICLES PERTAINING TO RESEARCH, NEWS AND INFORMATION FOR PARKINSON'S DISEASE, DEMENTIA, THE BRAIN, DEPRESSION AND PARKINSON'S WITH DYSTONIA. I ALSO POST ABOUT FUNDRAISING FOR PARKINSON'S DISEASE AND EVENTS. I TRY TO BE UP-TO-DATE AS POSSIBLE.

I AM NOT RESPONSIBLE FOR IT'S CONTENTS. I AM JUST A COPIER OF INFORMATION SEARCHED ON THE COMPUTER. PLEASE UNDERSTAND THE COPIES ARE JUST THAT, COPIES AND AT TIMES, I AM UNABLE TO ENLARGE THE WORDING OR KEEP IT UNIFORMED AS I WISH. IT IS IMPORTANT TO UNDERSTAND I AM A PERSON WITH PARKINSON'S DISEASE. I HAVE NO MEDICAL EDUCATION,

I JUST WANT TO SHARE WITH YOU WHAT I READ ON THE INTERNET. IT IS UP TO YOU TO DECIDE WHETHER TO READ IT AND TALK IT OVER WITH YOUR DOCTOR. I AM JUST THE COPIER OF DOCUMENTS FROM THE COMPUTER. I DO NOT HAVE PROOF OF FACT OR FICTION OF THE ARTICLE. I ALSO TRY TO PLACE A LINK AT THE BOTTOM OF EACH ARTICLE TO SHOW WHERE I RECEIVED THE INFORMATION SO THAT YOU MAY WANT TO VISIT THEIR SITE.

THIS IS FOR YOU TO READ AND TO ALWAYS KEEP AN OPEN MIND.

PLEASE DISCUSS THIS WITH YOUR DOCTOR, SHOULD YOU HAVE ANY QUESTIONS, OR CONCERNS. NEVER DO ANYTHING WITHOUT TALKING TO YOUR DOCTOR FIRST..

I DO NOT MAKE ANY MONEY FROM THIS WEBSITE. I VOLUNTEER MY TIME TO HELP ALL OF US TO BE INFORMED.

I WILL NOT ACCEPT ANY ADVERTISEMENT OR HEALING POWERS, HEALING FROM HERBS AND ETC. UNLESS IT HAS GONE THROUGH TRIALS AND APPROVED BY FDA. IT WILL GO INTO SPAM.

THIS IS A FREE SITE FOR ALL WITH NO ADVERTISEMENTS

THANK YOU FOR VISITING! TOGETHER WE CAN MAKE A DIFFERENCE!

TRANSLATE

Friday, December 11, 2015

Signaling from dysfunctional mitochondria induces a distinct type of senescence

Finding provides alternative explanation for the free-radical theory of aging and suggests new role for mitochondria in affecting physiology.

 
Buck Institute faculty Judith Campisi, PhD, says age researchers need to stop thinking of cellular senescence, now accepted as an important driver of aging, as a single phenotype that stems from genotoxic stress. Research from her lab reveals that cellular senescence, a process whereby cells permanently lose the ability to divide, is also induced by signaling from dysfunctional mitochondria - and that the arrested cells secrete a distinctly different "stew" of biologically active factors in a process unrelated to the damaging free radicals that are created in mitochondria as part of oxygen metabolism. The results are published in Cell Metabolism.
"We don't yet know how much this process contributes to natural aging," said Campisi, adding that those studies are currently underway. "But we do think the findings are important in addressing mitochondrial diseases, and those age-related diseases, such as some forms of Parkinson's, which involve mitochondrial dysfunction."
The discovery was unexpected and was made by postdoctoral fellow Christopher Wiley, PhD, who (in collaboration with Eric Verdin, PhD, from the Gladstone Institute) was eliminating sirtuins, a class of proteins long linked to longevity, one by one in human cell cultures. "The senescent phenotype only occurred when we eliminated the mitochondrial sirtuins," said Wiley. In addition, Wiley saw that the senescent cells secreted a different SASP (senescence-associated secretory phenotype) than expected - one that lacks the IL-1-dependent inflammatory arm - a major factor in the SASP originally identified in the Campisi lab in 2008. The authors dubbed this new phenomenon MiDAS - mitochondrial dysfunction-associated senescence.
Along with identifying MiDAS, Wiley also found that mitochondrial dysfunction upset the balance of NAD+ (an enzyme that is a co-factor for sirtuins), which arrested cell growth and prevented the IL-1-associated SASP. "The NAD+ balancing act happens outside the mitochondria in the cytoplasm of the cell," said Wiley. "This really highlights a signaling role for mitochondria, something understudied in the context of disease. And it identifies a new type of SASP, underscoring the existence of different types of senescence."
Wiley also identified the MiDAS SASP in mice genetically engineered to develop progeria in response to mitochondrial mutations, which causes rapid aging. The MiDAS SASP suppressed adipogenesis, which plays a vital role in metabolism and the creation of fat cells. He says the work provides a link to lipodystrophy, a medical condition characterized by abnormal or degenerative conditions involving fat tissue, adding that early HIV drugs (which are still being used in third world countries) deplete mitochondrial DNA and that patients receiving the drugs often show a particular loss of subcutaneous fat, especially in their face.
"For any disease that has a mitochondrial component this research adds a potential explanation for the real driver of the dysfunction -- and it's not free radicals, which we ruled out in our study" said Campisi. "Our finding suggest a new role for mitochondria when it comes to affecting physiology."
http://www.medicalnewstoday.com/releases/303946.php?tw

No comments:

Post a Comment