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Plastic chemical linked to smaller prefrontal cortex, reduced cognitive ability in rats

Findings demonstrate long-term influence of endocrine-disrupting compounds on brain development

Adult rats that had been exposed before birth and during nursing to a mixture of chemicals found in a wide range of consumer products have a smaller medial prefrontal cortex (mPFC) and perform worse on an attention-switching task than rats not exposed to the chemicals early in life. These findings, published in JNeurosci, demonstrate a long-term influence of endocrine-disrupting compounds on brain development.

Phthalates -- chemicals used in plastics belonging to the same class as Bisphenol A (BPA) -- can potentially interfere with hormones important for the developing brain.

Although previous studies have identified associations between phthalate exposure and developmental disturbances, little is known about the neurobiology underlying these relationships.

Janice Juraska and colleagues fed pregnant rats a daily cookie laced with human level doses of a chemical mixture based on data obtained from pregnant women. The researchers found both male and female adult offspring of these rats had fewer neurons and synapses in their mPFC and a specific deficit in cognitive flexibility.

As the mPFC is crucial for high level cognitive functions and reduced cognitive flexibility is observed in developmental disorders such as autism, the research shows how early life phthalate exposure can affect the brain and behavior.

Some answers to the sleep questions have been eye-opening. Bendlin and her colleagues identified 98 people from the registry who recorded their sleep quality and had brain scans. Those who slept badly — measured by such things as being tired during the day — tended to have more A-beta plaques visible on brain imaging, the researchers reported in 2015 in Neurobiology of Aging.

In a different subgroup of 101 people willing to have a spinal tap, poor sleep was associated with biological markers of Alzheimer’s in the spinal fluid, Bendlin’s team reported last year in Neurology. The markers included some related to A-beta plaques, as well as inflammation and the protein tau, which appears in higher levels in the brains of people with Alzheimer’s.

Bendlin’s studies are part of a modest but growing body of research suggesting that a sleep-deprived brain might be more vulnerable to Alzheimer’s disease. In animal studies, levels of plaque-forming A-beta plummet during sleep. Other research suggests that a snoozing brain runs the “clean cycle” to remove the day’s metabolic debris — notably A-beta — an action that might protect against the disease. Even one sleepless night appears to leave behind an excess of the troublesome protein fragment (SN Online: 7/10/17).

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