Lifeboat Foundation

As the world grapples with an aging population, the rise in neurodegenerative diseases such as Alzheimer’s and Parkinson’s is becoming a significant challenge. These conditions place a heavy burden not only on those afflicted but also on their families and society at large. Traditional treatments, including drug therapy and surgery, often come with side effects and high costs, and more critically, they fail to halt the progression of neuronal degeneration or prevent the death of neurons in patients.

Several studies have indicated that interrupted epigenetic reprogramming using Yamanaka transcription factors (OSKM) can rejuvenate cells from old laboratory animals and humans. However, the potential of OSKM-induced rejuvenation in brain tissue has been less explored. Here, we aimed to restore cognitive performance in 25.3-month-old female Sprague–Dawley rats using OSKM gene therapy for 39 days. Their progress was then compared with the cognitive performance of untreated 3.5-month-old rats as well as old control rats treated with a placebo adenovector. The Barnes maze test, used to assess cognitive performance, demonstrated enhanced cognitive abilities in old rats treated with OSKM compared to old control animals. In the treated old rats, there was a noticeable trend towards improved spatial memory relative to the old controls.

The treated mice were known as “supermodel grannies” in the lab because of their youthful appearance.

They were healthier, stronger and developed fewer cancers than their unmedicated peers.

The drug is already being tested in people, but whether it would have the same anti-ageing effect is unknown.

Turning off inflammatory protein extends healthy lifespan in mice.

A protein that promotes inflammation could hold the key to a longer, healthier life.

Humans also have the protein, called IL-11, offering hope for a future longevity treatment.

Continue reading “Mice live longer when inflammation-boosting protein is blocked” »

Identifying individuals who are at a high risk of age-related morbidities may aid in personalized medicine. Circulating proteins can discriminate disease cases from controls and delineate the risk of incident diagnoses^{1,2,3,4,5,6,7,8}. While singular protein markers offer insight into the mediators of disease^5,9,10,11, simultaneously harnessing multiple proteins may improve clinical utility¹². Clinically available non-omics scores such as QRISK typically profile the 10-year onset risk of a disease¹³. Proteomic scores have recently been trained on diabetes, cardiovascular and lifestyle traits as outcomes in 16,894 individuals¹⁴. Proteomic and metabolomic scores have also been developed for time-to-event outcomes, including all-cause mortality^{6,15,16,17,18,19,20,21}.

Here, we demonstrate how large-scale proteomic sampling can identify candidate protein targets and facilitate the prediction of leading age-related incident outcomes in mid to later life (see the study design summary in Extended Data Fig. 1). We used 1,468 Olink plasma protein measurements in 47,600 individuals (aged 40–70 years) available as part of the UK Biobank Pharma Proteomics Project (UKB-PPP)²². Cox proportional hazards (PH) models were used to characterize associations between each protein and 24 incident outcomes, ascertained through electronic health data linkage. Next, the dataset was randomly split into training and testing subsets to train proteomic scores (ProteinScores) and assess their utility for modeling either the 5-or 10-year onset of the 19 incident outcomes that had a minimum of 150 cases available. We modeled ProteinScores alongside clinical biomarkers, polygenic risk scores (PRS) and metabolomics measures to investigate how these markers may be used to augment risk stratification.

Researchers administered an injection of an anti-IL-11 antibody to 75-week-old mice, neutralizing the harmful effects of IL-11.

face_with_colon_three mitochondria immortality.

In a new study, lab mice given an experimental drug were jokingly referred to as “supermodel grannies” because they looked so youthful even while aging beyond their expected lifespan.

As the BBC reports, the trials for a drug believed to flush out a protein known as interleukin-11 — which in early development helps build our bones but later in life causes the kinds of inflammation that triggers much of the illness of aging — have already had intriguing success in mice.

Published in the journal Nature, a paper about the research undertaken by scientists at Imperial College London, Duke-NUS in Singapore, and the MRC Lab of Medical Sciences found that when given a drug that purges interleukin-11, the mice became more lean, had healthier fur, and had significantly lower levels of cancer than their counterparts of the same age.

– Read the column on Polytechnique Insights.