Changes in the Brain Associated with Alzheimer’s Disease Linked to Shortening of Telomeres
A new study led by Anya Topiwala of Oxford Population Health, part of the University of Oxford, UK, has revealed that changes in the brain caused by Alzheimer’s disease are associated with the shortening of the telomeres. The study was published on March 22 in the open-access journal PLOS ONE.
The Link between Telomeres and Aging
Telomeres are the protective caps on the ends of chromosomes that shorten as cells age. Telomeres on chromosomes protect DNA from degrading, but every time a cell divides, the telomeres lose some of their length. Short telomeres are a sign of stress and cellular aging and are also associated with a higher risk of neurological and psychiatric disorders.
The researchers compared telomere length in white blood cells to results from brain MRIs and electronic health records from more than 31,000 participants in the UK Biobank. The analysis revealed that patients with longer telomeres also tended to have better brain health. They had a larger volume of grey matter in their brains overall and a larger hippocampus, both of which shrink in patients with Alzheimer’s disease. The researchers speculate that longer telomeres might, therefore, help protect patients from developing dementia, though there was no association with stroke or Parkinson’s disease.
Implications of the Findings
Overall, the findings show that shorter telomeres can be linked to multiple changes in the brain associated with dementia. To date, this is the largest and richest study of the relationships between telomere length and MRI markers in the brain. The associations suggest that accelerated aging in the brain, as indicated by telomere length, could represent a biological pathway that leads to neurodegenerative disease. The authors add: “We found associations between telomere length, a marker of biological ageing, and multiple aspects of brain structure. This may explain why individuals with longer telomeres have a lower risk of dementia.”