Tag: Mitochondrial Dysfunction

Heart in body
The European Heart Journal has published a review of what happens to the human heart as it ages, noting the cellular effects of mitochondrial dysfunction and cellular senescence along with more visible changes such as hypertrophy and fibrosis. A constantly working organ The reviewers begin this paper by noting the constant work of the heart,...
Synapses
Scientists have discovered that ATP deficiency disrupts dopamine processing in synapses, leading to the accumulation of the harmful protein species that characterize Parkinson’s disease. ATP supplementation helps, but the road to the clinic might be long [1]. Parkinson’s and dopamine Parkinson's disease is defined by two hallmarks: the death of dopamine-producing neurons in a midbrain...
A mitochondrion
Researchers publishing in Nature Aging have described how mitochondrial stress is a key part of why senolytics are effective. Finding targeted effectiveness What Are Senolytics? Senotherapeutics for Senescent CellsSenolytics work by targeting one of several pro-survival pathways that senescent cells use to evade apoptosis and cling onto life. One of the challenges in dealing with...
Molybdenum sulfide
Scientists have created “nanoflowers” that nudge donor cells to produce more mitochondria, which can then be transferred to recipient cells to boost their mitochondrial function [1]. Mitochondrial transfer is difficult to improve Energy is required for life, and most energy in our cells is produced by mitochondria. When these organelles start to falter, it's a...
A new report from the Interventions Testing Program adds three new compounds to the list of lifespan-extending compounds confirmed during their experiments: epicatechin, halofuginone, and mitoglitazone [1]. Rigorous testing The National Institute on Aging’s Interventions Testing Program (ITP) is designed to rigorously test potential lifespan-extending compounds with a protocol that ensures reproducibility. In a standard investigation,...
Mitochondria
Scientists have discovered a possible mechanism behind age-related inflammation. It involves wrong building blocks being incorporated into mitochondrial DNA during replication and can be countered by adding the correct ones [1]. Too similar to bacteria Mitochondria, the cells’ energy-producing organelles, are considered to have developed from bacteria that once entered an ancient cell and stayed,...