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Research Roundup: MDMA signaling, brain imaging, alcohol metabolism

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Each week, The Daily’s Science & Tech section produces a roundup of the most exciting and influential research happening on campus or otherwise related to Stanford. Here’s our digest for the week of Dec. 8 – Dec. 14.

MDMA molecular signaling pathway identified

The molecular signaling pathway for the illicit drug commonly known as ecstasy or molly has been identified by Stanford researchers in a study published on Dec. 11 in “Science Translational Medicine.” Their findings elucidate distinctions between methylenedioxy-methamphetamine’s (MDMA) potential abuse and the potential for uses in treating post-traumatic stress disorder (PTSD) patients.

Led by Robert Malenka, psychiatry and behavioral sciences professor, the team is dedicated to finding treatments for psychiatric disorders and to discover methods to strengthen the patient-therapist relationship. MDMA’s effects include users feeling more social, which can lead to establishing trust levels between patient and therapist.

The researchers used mice in experiments to understand how they respond to MDMA by monitoring their behaviors with other mice. The findings suggested that MDMA triggers the release of serotonin, thus influencing mice to become more sociable.

“We’ve figured out how MDMA promotes social interaction and showed that’s distinct from how it generates abuse potential among its users,” Malenka told Stanford Medicine News.

Children with diabetes exhibit different brain patterns when performing cognitive tasks

Children with Type 1 diabetes have different brain patterns than those without the disease, a study published by Stanford researchers on Dec. 9 in “Public Library of Science Medicine” found.

“Our findings suggest that, in children with Type 1 diabetes, the brain isn’t being as efficient as it could,” Lara Foland-Ross, senior research associate at the Center for Interdisciplinary Brain Sciences Research, told Stanford Medicine News.

The researchers evaluated patients between 7 to 14 years of age with a functional magnetic resonance imaging (fMRI) while they performed a cognitive task. Children with diabetes had different fMRI brain patterns than children without the disease, and the abnormal imaging is similar to patients affected with a cognitive decline in aging, concussion, attention-deficit hyperactivity disorder and multiple sclerosis.

“The takeaway from our study is that, despite a lot of attention from endocrinologists to this group of patients, and real improvements in clinical guidelines, children with diabetes are still at risk of having learning and behavioral issues that are likely associated with their disease,” Allan Reiss, psychiatry and behavioral sciences professor, told Stanford Medicine News.

‘Asian glow’ alcohol metabolism mutation can lead to Alzheimer’s development

A common mutation involved with incomplete alcohol metabolism can lead to an increased risk of developing Alzheimer’s disease, a study published on Dec. 12 in “Acta Neuropathologica Communications” found.

The mutation, sometimes called “Asian glow,” is in the aldehyde dehydrogenase 2 gene (ALDH2), associated with a reaction where the face turns red after alcohol consumption. This results from the buildup of acetaldehyde, a toxic byproduct of incomplete alcohol metabolism.

“Our data suggest that alcohol and Alzheimer’s disease-prone genes may put humans at greater risk of Alzheimer’s onset and progression,” Daria Mochly-Rosen, chemical and systems biology professor, told Stanford Medicine News.

The researchers used cells from human patients and mice for their experiments between ALDH2 and alcohol consumption. Protein from the mutated gene had a limited ability to break down acetaldehyde.

The findings suggested in human-derived cells and mice with the mutated gene, more free radicals were not removed from the cells or mice. Free radicals are unstable atoms, and too many free radicals can cause damage to the mitochondria. This is commonly associated with death of neurons, leading to Alzheimer’s disease.

“These free radicals form toxic aldehydes, and the job of ALDH2 is to remove these toxic chemicals,” Mochly-Rosen told Stanford Medicine News. “Once these aldehydes accumulate, the first organelles that they damage are the organelles that contain the enzyme that is supposed to get rid of them: the mitochondria.”

The researchers also discovered that adding Alda-1, a small molecule, can restore function of the mutated enzyme.

“This is based on our patient-derived cell studies and our animal studies, so an epidemiological study in humans should be carried out in the future,” Mochly-Rosen told Stanford Medicine News.

Contact Derek Chen at derekc8 ‘at’ stanford.edu.

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