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DISCOVERIES

NEUROSCIENCE

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.

NEW NEURONS

REVEAL CLUES

ABOUT AUTISM

SMALL MOLECULE KEEPS NEW

ADULT NEURONS FROM STRAYING,

MAY BE TIED TO SCHIZOPHRENIA

Neurons derived from cells of people with

autism spectrum disorder show specific defects

compared with those neurons derived from

healthy people, including diminished ability to

form excitatory connections with other neurons

(indicated by red and green dots in the neuron).

MicroRNA miR-19 helps budding

adult brain cells stay on track. Over-

expressing miR-19 microRNA in neural

progenitor cells in the adult brain of

mice caused new neurons (green) to

move and branch abnormally (right)

compared to control neurons (left).

A small stretch of ribonucleic acid

called microRNA could make the

difference between a healthy adult

brain and one that’s prone to disorders

including schizophrenia.

Scientists at the Salk Institute

discovered that miR-19 guides the

placement of new neurons in the adult

brain, and the molecule is disrupted in

cells from patients with schizophrenia.

The findings, published in the journal

Neuron

on July 6, 2016, pave the way

toward a better understanding of how

the adult brain controls the growth of

new neurons and how it can go wrong.

Salk Professor Rusty Gage, first author

Jinju Han and their colleagues found

that levels of miR-19 changed more than

levels of any other microRNAwhen

precursors to new brain cells in these

areas (called neural progenitor cells)

were coaxed to become neurons in the

adult brain. The researchers went on to

show that when miR-19 was blocked in

neural progenitor cells, levels of RNA

corresponding to a gene called Rapgef2

were altered. Moreover, new neurons

did not migrate to the correct areas of

the brain.

Because the incorrect migration of

new brain cells has been implicated

in neuropsychiatric disorders like

schizophrenia, Gage’s group next

analyzed the levels of miR-19 and

Rapgef2 in neural progenitor cells that

had been created by reprogramming

skin cells from schizophrenic patients.

Although the patients had no mutations

in the gene for Rapgef2, they had high

levels of miR-19 that corresponded with

low levels of both the RNA and protein

for Rapgef2. The team is now studying

the role of miR-19 in mouse models of

schizophrenia, as well as looking at cells

from broader cohorts of human patients.

8 INSIDE SALK

WINTER 2016

WWW.SALK.EDU