Unlocking the Mystery: How Evolution Sheds Light on Rising Autism Rates in Humans

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Unlocking the Mystery: How Evolution Sheds Light on Rising Autism Rates in Humans

A recent study published in Molecular Biology and Evolution explores how human evolution may explain rising rates of autism spectrum disorder (ASD). The research suggests that certain brain cells in humans evolved quickly compared to other primates, which might be linked to ASD prevalence.

Currently, about 1 in 31 children in the U.S., or roughly 3.2%, has been diagnosed with autism. Globally, the World Health Organization estimates that around 1 in 100 children is affected. Interestingly, signs of autism and related conditions are almost absent in non-human primates, indicating these traits may be unique to humans.

The study utilized single-cell RNA sequencing to uncover diverse brain cell types. It highlighted significant genetic changes in humans, suggesting that specific cells, particularly L2/3 IT neurons, evolved rapidly. This acceleration may relate to genes associated with autism, hinting that natural selection favored these traits in our ancestors.

Lead author Alexander L. Starr mentions, “Our results suggest that some of the same genetic changes that make the human brain unique also made humans more neurodiverse.” This notion raises questions about how traits linked to autism, such as developmental delays, may have benefited early humans by allowing for more extensive brain development and complex thinking.

An important perspective here is that the extended time for brain development in children might have led to enhanced communication skills, further aiding human survival and social interaction. However, what exactly conferred fitness benefits through these traits remains unclear.

As autism rates continue to rise, understanding its roots in our evolution offers a fascinating lens. It reminds us that diversity in the human brain has its place in our history—and could shape our future.

For further details, check out the study by Alexander L. Starr et al., which can be accessed here.



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