Clearance of p16Ink4a-positive senescent cells delays ageing-associated disorders

This might just help your recovery from stroke, won't know until human research is accomplished. Your doctor and stroke hospital can once again completely fail at contacting researchers to get clinical trials done.  Of the thousands of research articles I've cited has your stroke hospital done ONE DAMN THING with any of them? Created protocols? Initiated research? Nope? Then you need to start firings with the board of directors. 

 Quotes from the article referencing the research; 'If we can clear senescent cells, then we can probably clear Alzheimer's'. 'Maybe we can remove senescent astrocytes and finally get some headway on Alzheimer's'.

From 'Why Alzheimer's hits older brains' New Scientist, Sept. 29, 2012

Clearance of p16^Ink4a-positive senescent cells delays ageing-associated disorders

• Darren J. Baker,
• Tobias Wijshake,
• Tamar Tchkonia,
• Nathan K. LeBrasseur,
• Bennett G. Childs,
• Bart van de Sluis,
• James L. Kirkland &
• Jan M. van Deursen 

Nature volume 479, pages232–236(2011)Cite this article

• 11k Accesses
• 1293 Citations
• 589 Altmetric
• Metrics details

Abstract

Advanced age is the main risk factor for most chronic diseases and functional deficits in humans, but the fundamental mechanisms that drive ageing remain largely unknown, impeding the development of interventions that might delay or prevent age-related disorders and maximize healthy lifespan. Cellular senescence, which halts the proliferation of damaged or dysfunctional cells, is an important mechanism to constrain the malignant progression of tumour cells^1,2. Senescent cells accumulate in various tissues and organs with ageing³ and have been hypothesized to disrupt tissue structure and function because of the components they secrete^4,5. However, whether senescent cells are causally implicated in age-related dysfunction and whether their removal is beneficial has remained unknown. To address these fundamental questions, we made use of a biomarker for senescence, p16^Ink4a, to design a novel transgene, INK-ATTAC, for inducible elimination of p16^Ink4a-positive senescent cells upon administration of a drug. Here we show that in the BubR1 progeroid mouse background, INK-ATTAC removes p16^Ink4a-positive senescent cells upon drug treatment. In tissues—such as adipose tissue, skeletal muscle and eye—in which p16^Ink4a contributes to the acquisition of age-related pathologies, life-long removal of p16^Ink4a-expressing cells delayed onset of these phenotypes. Furthermore, late-life clearance attenuated progression of already established age-related disorders. These data indicate that cellular senescence is causally implicated in generating age-related phenotypes and that removal of senescent cells can prevent or delay tissue dysfunction and extend healthspan.

Access options

Subscribe to Journal

Get full journal access for 1 year

$199.00

only $3.90 per issue

Subscribe

All prices are NET prices.
VAT will be added later in the checkout.

Rent or Buy article

Get time limited or full article access on ReadCube.

from$8.99