SCIENCE
Drugs and Telomeres: A New Look at Autism Treatment
Thu Apr 24 2025
Telomeres are tiny parts of our chromosomes that get shorter as we age. They play a big role in how our cells age and work. Scientists have found that people with autism spectrum disorder (ASD) often have shorter telomeres. This has led researchers to wonder if the drugs used to treat ASD might affect telomere length.
In a recent study, researchers used rats to explore this idea. They gave the rats a substance called valproic acid (VPA) to mimic some aspects of ASD. Then, they treated these rats with three different drugs: amitriptyline, risperidone, and nooclerin. These drugs are often used to help manage symptoms in people with ASD.
The researchers looked at telomere length and the activity of certain genes in the rats' blood cells, prefrontal cortex, and hippocampus. These genes are involved in maintaining telomeres. They found that risperidone and nooclerin had some interesting effects.
Risperidone, for instance, made telomeres longer in male rats' blood cells. It also boosted the activity of certain genes in the prefrontal cortex. Nooclerin had a similar effect on telomere length in male rats' blood cells and increased the activity of a specific gene.
The study also found some connections between telomere length, gene activity, and behavior. Longer telomeres in male rats' blood cells were linked to less anxiety. Interestingly, the activity of a gene called Tpp1 was connected to repetitive behaviors in both male and female rats.
These findings suggest that some ASD treatments might influence telomere length and gene activity in a way that depends on the rat's sex. This could give scientists new clues about how ASD affects the brain and how to treat it.
However, it's important to note that this study was done on rats, not humans. While rats share many biological similarities with humans, they are not the same. More research is needed to see if these findings apply to people with ASD.
Moreover, the study only looked at a few drugs and a specific set of genes. There are many other drugs and genes that could be involved. Future studies should explore these factors to get a more complete picture.
Lastly, the study used VPA to mimic ASD, which is not the same as having ASD. VPA affects the body in specific ways that might not be the same as the causes of ASD. Therefore, the results might not fully represent what happens in people with ASD.
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questions
How do the observed sex-dependent effects of nooclerin and risperidone on telomere length inform future personalized treatment strategies for ASD?
What are the potential biases in using the VPA rodent model to study telomere dynamics in ASD?
What other factors, besides the drugs tested, could influence telomere length and gene expression in the studied rat models?
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