AI Article Synopsis
- Telomeres, which are protective caps on chromosomes, generally shorten in white blood cells as people age, which is a risk factor for neurodegenerative diseases.
- The connection between shorter leukocyte telomere length (LTL) and diseases like Alzheimer's and Parkinson's is unclear, with research showing mixed results.
- More studies are necessary to explore how telomeres in brain cells behave during aging and disease, and to investigate whether telomere shortening directly contributes to or worsens neurological conditions.
Article Abstract
Telomeres, ribonucleoprotein complexes that cap eukaryotic chromosomes, typically shorten in leukocytes with aging. Aging is a primary risk factor for neurodegenerative disease (ND), and a common assumption has arisen that leukocyte telomere length (LTL) can serve as a predictor of neurological disease. However, the evidence for shorter LTL in Alzheimer's and Parkinson's patients is inconsistent. The diverse causes of telomere shortening may explain variability in LTL between studies and individuals. Additional research is needed to determine whether neuronal and glial telomeres shorten during aging and in neurodegenerative disorders, if and how LTL is related to brain cell telomere shortening, and whether telomere shortening plays a causal role in or exacerbates neurological disorders.
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Source |
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| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC4008659 | PMC |
| http://dx.doi.org/10.1016/j.tins.2014.02.010 | DOI Listing |
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