Mitochondrial Performance May Strongly Influence Learning

Despite considerable and growing effort put towards the development of novel means to slow and reverse aging over the past thirty years, the longest lived laboratory mice remain those lineages first established in the 1990s with mutations that disable growth hormone metabolism…

Tobacco smoking is a critical modifiable risk factor for age-related diseases and mortality. Although smoking cessation is known to improve health outcomes, whether smoking-induced biological aging is reversible upon cessation remains unclear.

Researchers have been working towards practical approaches to inhibiting RUNX2 activity as a way to slow age-related loss of bone mineral density. Bone extracellular matrix is constantly remodeled throughout life, created by osteoblast cells and destroyed by osteoclast cells.

A new atlas identifies 1,067 unannotated microproteins in the human frontal cortex with strong spectral grades. A subset is differentially expressed in Alzheimer’s disease independently of their canonical genes, including an MKKS-derived microprotein required for normal microglial mitochondrial respiration.

Microproteins, small proteins of 100–150 amino acids, are largely absent from reference proteomes and have been overlooked in brain and aging research.

Aged mice showed substantial individual variability in cognitive inflexibility, associated with greater abundance of synapse-associated mitochondrial proteins in the medial prefrontal cortex.

Cancer rates are rising in adults under 55, and new research suggests accelerated biological aging may be one piece of the puzzle.

Scientists have discovered that the brain’s short-range wiring may help protect cognition even as gray matter shrinks with age. Healthier connections just beneath the brain’s surface were linked to better language skills and appeared to weaken the impact of gray matter loss.

“I mean we have the knowledge to prevent heart disease now. It's applying it earlier in life that really makes the difference. That's my pitch to the 30-year-old, and there's a lot of pushback.”‒ Michael Davidson

Sleep is increasingly recognised as a potentially modifiable factor in cognitive ageing, but evidence is often limited by cross-sectional designs, single sleep measures and global cognitive outcomes.