Checkout the latest Longevity Reporter Newsletter (15th August, 2015), covering this week’s top news in health, aging, longevity
This week: ‘Danielle’ — An Eye Opening Simulation Of The Aging Process; How Does Chronic Inflammation Lead To Cancer?; Low Inflammation and Telomere Maintenance Predict Healthy Longevity; 3-D Printing: Could Downloadable Medicine Be The Future?; And more.
“A protein found in the blood of young animals called GDF-11 is inducing systemic rejuvenation effects on bone, muscle, heart, blood vessels, and brains of older animals.
“GDF” stands for growth differentiating factor. It functions to turn “on” senescent stem cells, which results in a restoration of youthful structure and function to senile tissues. This same protein (GDF-11) is found in young humans as well as animals.
Harvard, Stanford, and other universities are conducting remarkable studies showing age reversal in animal models. Researchers from these centers of medical innovation are optimistic that this approach might be applicable to humans.”
Reversing aging may be humanly possible. It may also be closer than you think.
At Inman Connect San Francisco, Dr. Aubrey de Grey, the chief science officer at SENS Research Foundation, talked about disrupting death.
A universal therapy that targets mis-folded proteins is a very significant step forward if clinical trials in humans translate from animals. Obviously there is more work to be done but it this is the kind of technology we need in order to intervene against biological aging.
It is not hard to see that a therapy like this followed up by another that regenerates the brain eg, the Conboy Lab work by promoting neurogenesis could be a way to repair and restore the brain to healthy function.
A drug that breaks up different types of brain plaque shows promising results in animals and could prevent Alzheimer’s and Parkinson’s disease.
The decline of the thymus, responsible for the upkeep of our adaptive immune system, might be due to oxidative damage and insufficient antioxidant mechanisms to combat it.
What if “life in prison” could mean 100 or 200 or 400 years? Does that change the way that sentences are doled out? What happens when a person gets out of prison?
For all of you who’ve written in asking me to do an episode about longevity, this episode is for you. But instead of looking at the usual living forever stuff, we’re specifically going to talk about what happens when it gets applied to the prison system.
While exploring which biological processes might predict successful in centenarians, a team from Newcastle and Tokyo have identified two prominent factors that facilitate health longevity — low level inflammation and telomere length.
“Centenarians and supercentenarians are different — put simply, they age slower. They can ward off diseases for much longer than the general population.”
After measuring a number of health markers in 1,554 people including: those over 105, between 100 and 105 and a group near their 100th birthday along with their offspring, these two elements emerged as consistent longevity predictors.
This is an interesting story in one of Italy’s top 3 papers/sites about life extension science and millennials living beyond 100 years of age. It also features transhumanism: http://numerus.corriere.it/2015/08/06/i-millennials-camperanno-centanni-o-anche-piu-ma-se-lo-potranno-permettere/ and the English: https://translate.google.com/translate?hl=en&sl=it&u=http://numerus.corriere.it/2015/08/06/i-millennials-camperanno-centanni-o-anche-piu-ma-se-lo-potranno-permettere/&prev=search
Le tendenze della statistica ci dicono che chi oggi ha vent’anni ha ottime probabilità di arrivare ai cento in buona salute. Forse anche molto di più, se avranno successo le battaglie del Partito Transumanista che si presenta alle elezioni americane del 2016 con l’obiettivo di puntare più risorse sulla lotta all’invecchiamento. Ma come si configura un mondo di persone tanto longeve? L’allungamento della vita potrà beneficiare tutte le popolazioni o soltanto una fascia di privilegiati? Già oggi la speranza di vita nei Paesi più poveri è mediamente inferiore di 18 anni rispetto ai Paesi più ricchi e anche in Italia ci sono tre anni di differenza tra Milano e Napoli. E come si ridisegna un sistema sociale nel quale le persone vivranno venti o trent’anni più di oggi?
Un autobus rosso a forma di bara, con tanto di fiori finti sul tetto, percorre le strade degli Stati Uniti. Lo ha voluto il leader del Partito transumanista Zoltan Istvan, candidato alle elezioni presidenziali del 2016. Istvan non diventerà presidente, ma il suo messaggio non è banale: con il suo tour elettorale, vuole attirare l’attenzione sulla battaglia contro l’invecchiamento. Chiede più fondi per la ricerca e per le cure sanitarie, più carriere nelle attività tecnologiche, nell’intelligenza artificiale e nella medicina.
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Eating a group of specific foods — known as the MIND diet — may slow cognitive decline among aging adults, even when the person is not at risk of developing Alzheimer’s disease, according to researchers at Rush University Medical Center.
This finding supplements a previous study by the research team, reported by KurzweiliAI in March, that found that the MIND diet may reduce a person’s risk in developing Alzheimer’s disease.
The researchers’ new study shows that older adults who followed the MIND diet more rigorously showed an equivalent of being 7.5 years younger cognitively than those who followed the diet least. Results of the study were recently published online in the journal Alzheimer’s & Dementia: The Journal of the Alzheimer’s Association.
As the brain ages, it becomes less efficient at recycling and eliminating build up of waste; ‘removal vans’ fail to do the rounds, and accumulation starts to overtake removal.
“We found that people in their 30s typically take about four hours to clear half the amyloid beta 42 from the brain,” says Randall J. Bateman. “In this new study, we show that at over 80 years old, it takes more than 10 hours.”
Research has uncovered that a protein called amyloid beta 42 (a natural byproduct of neural activity), is normally removed effectively in youth but the rate of clearance was found to slow progressively with age. Accumulation of amyloid beta 42 can lead to aggregation and consequent plaque formation and a slowdown in removal was tied to symptoms of dysfunction including memory loss and personality change. The study found that the brain disposes of this protein through a number of channels, and more work could uncover ways of boosting waste mangement in ailing brains, thus avoiding this toxic accumulation.