Neuroscience

Salk Professor David Schubert, first author Antonio Currais and collaborators uncovered preliminary evidence that tetrahydrocannabinol (THC) and other compounds found in marijuana can promote the cellular removal of amyloid beta, a toxic protein associated with Alzheimer’s disease. While these exploratory studies, detailed in Aging and Mechanisms of Disease, were conducted in neurons grown in the laboratory, they may offer insight into the role of inflammation in Alzheimer’s and could provide clues to developing novel therapeutics for the disorder.

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A Neuron study from John Reynolds‘ lab reveals more about how the brain processes vision, which could contribute to new therapies or visual prosthetics. Bursts in a neuron’s electrical activity—the number of “spikes” that result when brain cells fire—make up the basic code for perception, according to traditional thought. But neurons constantly speed up and slow down their signals. Reynolds, first author Anirvan Nandy and colleagues found that being able to see the world relies on not just the number of spikes but the timing of those spikes as well.

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The brains of some people with autism spectrum disorder grow faster than usual early on in life, often before diagnosis. In a study co-led by the Salk Institute, researchers found that stem cell-derived neurons made fewer connections in the dish compared to cells from healthy individuals. Furthermore, the scientists were able to restore communication between the cells by adding IGF-1, a drug currently being evaluated in clinical trials of autism.

In the journal Molecular Psychiatry, Salk Professor Rusty Gage, first author Carol Marchetto and colleagues show that it is possible to use stem cell reprogramming technologies developed in the past decade to model the earliest stages of complex disorders and to evaluate potential therapeutic drugs.

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In an August 2016 Nature paper spanning molecular genetics, stem cells and the sciences of brain and behavior, researchers at the University of California, San Diego and the Salk Institute have created a neurodevelopmental model of a rare genetic disorder that may provide new insights into the underlying neurobiology of the human social brain. The disorder, called Williams syndrome (WS), is a rare genetic condition caused by deletion of one copy of 25 contiguous genes on chromosome 7, out of an estimated 30,000 genes in the brain.

Alan Saghatelian’s lab identified a new connection between a gene called ApoE4 and protein build-up associated with Alzheimer’s. Previous reports have suggested that ApoE4 may affect how the brain clears out protein clusters called betaamyloid plaques, but what was happening at the molecular level wasn’t clear. Saghatelian, first author Qian Chu and colleagues pinpointed how an enzyme, HtrA1, degrades ApoE4, which can let researchers better test hypotheses about ApoE4’s role in Alzheimer’s. The findings appear in the Journal of the American Chemical Society.

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Xin Jin and colleagues are using cutting-edge genetic, electrophysiological, and neural-tracing strategies to delve into the anatomy and function of lesser-known forms of organization in the brain. Jin, together with the paper’s first authors Jared Smith, Jason Klug and Danica Ross, unraveled how particular cells in an area called the striatum receive a complex variety of information. This work, published in Neuron, could help better understand disorders such as Parkinson’s disease, obsessive-compulsive disorder or addiction.

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The lab of Kuo-Fen Lee found that boosting levels of a specific protein in the brain alleviates hallmark features of Alzheimer’s disease in a mouse model of the disorder. The protein, called neuregulin-1, has many forms and functions across the brain and is already a potential target for treating brain disorders, as detailed by Lee and first author Jiqing Xu on August 25, 2016 in Scientific Reports.

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