A Mechanistic Explanation for SIRT1’s Effects

Aging clocks can be readily produced by using what are by now well established machine learning techniques on any body of biological data that changes with age.

Here, researchers report on their investigation of gene therapy to introduce a bacterial enzyme, lipoic acid protein ligase A (LplA), into mammals in order to improve mitochondrial metabolism.

One might think that an alteration to the machinery of gene expression that systemically changes the amino acid components of proteins, in effect giving all proteins the possibility of multiple single nucleotide polymorphisms, would be quite harmful.

Yadav et al. develop a framework that quantifies tissue structural aging without training on chronological age, using a large dataset of human histology images. They reveal distinct yet coordinated organ aging trajectories, and link accelerated aging to pathways, genetic variants and pathology.

Lifestyle interventions can preserve the independence of older adults. Here the authors show that multimorbidity patterns influenced the efficacy of a multicomponent lifestyle intervention targeting mobility disability in frail older adults.

Assisting an ageing loved one can start with small tasks but may lead to full-time caregiving that requires more support Helping an ageing parent or loved one often begins with easy-to-field requests: Pick up a prescription. Drive them to a doctor’s appointment.

As dogs age, many develop more than one chronic health condition.

“People should have hope, in the sense that it's very important to be as empowered as possible by keeping a log of information, by providing their clinicians or the treating physicians or providers with the details of their headache, and recognizing the…

To investigate associations between body roundness index (BRI) and progression of cardio-renal-metabolic diseases (CRMDs). This study included 442,489 UK Biobank participants aged ≥ 40 years without CRMDs at baseline. BRI was analyzed continuously and by tertiles.

Pulmonary hypertension (PH) frequently complicates heart failure with reduced ejection fraction (HFrEF), worsening prognosis despite limited therapeutic options. Whether sodium-glucose cotransporter 2 inhibitors (SGLT2i) improve PH beyond their established hemodynamic effects remains unclear.