BubR1 Protein, Stem Cells, and Cell Senescence

Researchers are studying the role of the BubR1 protein and cellular senescence in adult stem cells.

Cellular senescence is the condition where a cell loses its ability to divide. Although they are no longer able to replicate, these cells are still metabolically active.

Senescent cells are cells that are attributed to aging. They are associated with features such as wrinkles and dry skin. Some cells become senescent after undergoing fifty cell division cycles (called the Hayflick phenomenon) or through other factors such as harmful toxins or damage to its DNA. For DNA related cellular senescence, the ends of DNA strands that shorter and shorter after each cell division. Once the ends called telomeres are used up, the actual genetic strands get damaged. This is when the cells stops dividing.

Senescence is an irreversible process and scientists are studying this phenomenon in relation to aging and the growth of cancerous tumors. Studies show that when senescent cells are purposely removed, it can prevent or delay tissue degradation and extend the healthspan of the body.

Cellular Structure
Credit: Wikipedia

Studying Cell Senescence And Its Relation To The Aging Of the Brain

Senescence is the change in the form and biology of a cell or organism as it ages past its maturity. When a cell loses its ability to divide, this is called cellular senescence. It must be noted that with cellular senescence, the affected cell is still metabolically active. These are called senescent cells.

Senescent cells exhibit changes in form and function which may lead to age-related changes such as wrinkles and surface dryness. Some cells become senescent after an average of 50 cycles of replication or division. Other cells become senescent because of exposure to toxins or DNA damage.

Senescence is an irreversible process and scientists are studying this phenomenon in relation to aging and the growth of cancerous tumors.

Scientists discover how the brain ages

The ageing process has its roots deep within the cells and molecules that make up our bodies. Experts have previously identified the molecular pathway that react to cell damage and stems the cell's ability to divide, known as cell senescence.

However, in cells that do not have this ability to divide, such as neurons in the brain and elsewhere, little was understood of the ageing process. Now a team of scientists at Newcastle University, led by Professor Thomas von Zglinicki have shown that these cells follow the same pathway.

This challenges previous assumptions on cell senescence and opens new areas to explore in terms of treatments for conditions such as dementia, motor neuron disease or age-related hearing loss.