Video

Coca-Cola 100-Year-Old Man Shares the Secret to Happiness (w/ English subtitles)

Saga

In an issue of Science (2 December 2011), Jennifer Couzin-Frankel wrote a piece about the story of sirtuins and other ageing-related genes and molecules. It all began in the lab of Leonard Guarente (at MIT), around 1998. Leonard’s group presented the idea that there could be a set of genes linked to the lifespan-extending effect of calorie restriction. Many years have passed, many more people got involved and got interested, yet the controversies, arguments, conflicting results, and discussions continue to linger. The most recent finding came from Matt Kaeberlein and his colleagues, in which they confirmed no effects of a key ageing gene in invertebrate animals like worms and flies.

Dame Edna on ageing

In a recent interview with  the FT, Barry Humphries describes getting old as depressing. With the numerous things to do on his list, he says that he has to cross off some of it: some books to read, some places to visit. He admits that he will probably be unable to read the complete works of George Meredith. He adds that he will never be able to go on a walking tour of Patagonia, nor a picnic in Mongolia. He has completely crossed China off his list too.

 

genetic cause of two neurological diseases (ALS and FTD)

Researchers have identified a repeat expansion in C9ORF72 as the genetic defect on chromosome 9p21 responsible for frontotemporal dementia (FTD) and amyotrophic lateral sclerosis (ALS).

Renton et al.  A Hexanucleotide Repeat Expansion in C9ORF72 Is the Cause of Chromosome 9p21-Linked ALS-FTD

DeJesus-Hernandez et al.  Expanded GGGGCC Hexanucleotide Repeat in Noncoding Region of C9ORF72 Causes Chromosome 9p-Linked FTD and ALS

upcoming lecture: cognition and ageing

If you happen to be in London next month, why not drop by at The British Academy, 10-11 Carlton House Terrace, SW1Y 5AH. Professor Lorraine Tyler is scheduled to give the joint British Academy and British Psychological Society Lecture on September 22, 2011 (Tuesday, 6.00pm – 7.15pm). [link]

reversibility of memory loss

Yale researchers show how memory is lost and found.

In a recent journal article, Min Wang and colleagues described that memory loss as a consequence of age-related decline in persistent neuronal firing can be rescued by restoring an optimal neurochemical environment.

[video]

the ageing suit

James Crabtree wrote a piece on the FT, check it out:

http://www.ft.com/intl/cms/s/2/1fed1eee-b34b-11e0-9af2-00144feabdc0.html

many nations have graying populations

John Timmer (Ars Tecnica) wrote a piece about the increasing old population in developing countries. He described caring for the elderly as one of the biggest challenges of global health. He cited one of the key discussions from the recent Lindau Nobel Laureates Meeting: majority of the world’s nations now look very much like the industrialized world, with small family sizes and life expectancies of around 70 years and up.

Check it out … http://arst.ch/q6l

100

Here’s a very nice video clip of 100th birthday celebration – 100

the common biology of cancer and ageing

Let us revisit the review paper by Toren Finkel and colleagues in which they discussed “key observations that has led to a complex but growing convergence between our understanding of the biology of ageing and the mechanisms that underlie cancer” (Nature 448, 767-774 | 16 August 2007 | doi:10.1038/nature05985).

At the end, they presented a model that views ageing and cancer from a stem-cell-biology perspective:

“Over the lifespan of an organism, long-lived cells (such as stem cells) accumulate DNA damage from a number of stresses including intracellular oxidants generated from normal metabolism. The default pathway for such damaged stem cells is to undergo growth arrest, apoptosis or senescence. As more and more stem cells withdraw from the proliferative pool, there is a decrease in the overall number and/or functionality of both stem and progenitor cells. This decrease predisposes the organism to impaired tissue homeostasis and regenerative capacity and could contribute to ageing and age-related pathologies. Presumably, some rare cells can escape from this normal default pathway by acquiring additional mutations that allow them to continue to proliferate even in the setting of damaged DNA. These proliferating but damaged cells might provide the seeds for future malignancies. In this scenario, both cancer and ageing result primarily from accumulating damage to the stem and progenitor cell compartment. Mutations that allow stem cells to continue to proliferate in the setting of normal growth arrest signals such as DNA damage (for example, loss of p16INK4a or reactivation of telomerase) would temporarily expand the stem cell pool and hence delay age-related pathologies. Over the long term, these mutations would also increase the likelihood of cancer.”