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INSIDE SALK

WINTER 2016

WWW.SALK.EDU

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.

Salk scientists map brain’s

action center

NEURON

08/2016

Cannabinoids remove plaque-

forming Alzheimer’s proteins

from brain cells

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 andMechanisms

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.

AGING AND

MECHANISMS

OF DISEASE

06/2016

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

.

Elevating brain protein allays

symptoms of Alzheimer’s and

improves memory

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 beta-

amyloid 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

.

Newmechanism discovered

for Alzheimer’s risk gene

JOURNAL OF

THE AMERICAN

CHEMICAL

SOCIETY

08/2016

SCIENTIFIC

REPORTS

08/2016