Exploring The Causal Relationship Between Telomere Regulation, Aging And Neurological Disorders
Our bodies are made of countless cells, and inside each cell are chromosomes that carry our genetic information. At the ends of these chromosomes are protective caps called telomeres. Think of them like the plastic tips on shoelaces, preventing the shoelaces from fraying. Every time a cell divides, these telomeres get a little shorter. This natural shortening, often called telomere attrition, is a key indicator of biological aging.
As we age, our telomeres naturally shorten, and this process has been linked to a higher risk of developing various age-related conditions, including serious brain disorders. Scientists are exploring how this shortening might contribute to conditions like Alzheimer’s disease, Parkinson’s disease, multiple sclerosis, stroke, and even brain tumors.
When telomeres become too short, cells can no longer divide and may enter a state of “senescence” or even die. This can lead to problems like neurodegeneration, which is the progressive loss of brain cells, and immune senescence, where our immune system becomes less effective at fighting off diseases. It can also contribute to cerebrovascular dysfunction, meaning issues with the blood vessels in the brain.
While the exact cause-and-effect relationship between telomere shortening and these neurological disorders is still being investigated, understanding telomere biology offers exciting possibilities. Researchers are looking into whether telomere length could serve as an early warning sign or “biomarker” for disease progression. Furthermore, therapies that aim to modify telomere length, such as activating or inhibiting the enzyme telomerase (which helps maintain telomeres), are being explored as potential new strategies to protect the brain and combat these debilitating conditions.
Source: link to paper