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JNeurosci: Highlights from the Jan. 18 issue

January 18, 2017

Genetic Variation Linked to Alzheimer's Plays Opposite Roles in Early and Late Stages of Disease

One of the strongest genetic risk factors for the development of Alzheimer's disease is a variation in an immune-related gene. The gene -- TREM2 -- codes for a receptor found only on the brain's immune cells, but recent studies investigating its role in Alzheimer's have yielded conflicting results. In a new study in mice, researchers find TREM2 plays opposite roles in Alzheimer's pathology in early and late stages of the disease. The findings shed light on immune function in the Alzheimer's brain and suggest therapies targeting neuroinflammation should take disease stage into account.

Gary Landreth,

Chronic Pain May Alter Endocannabinoid Signaling in Brain

Endocannabinoids -- innate molecules that regulate how neurons function -- bind to sites in a key brain pathway to reduce pain. In a new study in rats, researchers find chronic pain alters endocannabinoid signaling in this pathway. They also find activity of a specific cannabinoid receptor is elevated in persistent inflammation, suggesting drugs targeting these sites may be useful in treating chronic inflammatory pain.

Ming-Hua Li,

Epigenetic Changes May Exacerbate Neuropathic Pain After Nerve Injury

Nerve injuries can produce long-lasting and debilitating neuropathic pain. Injury alters the way certain genes are expressed in sensory neurons in the spinal cord, and these changes may contribute to chronic neuropathic pain. In a new study in mice, researchers find alterations in gene expression after spinal nerve injury increases the amount of a proinflammatory molecule in the spinal cord, worsening symptoms of neuropathic pain.

Yong-Jing Gao,
The Journal of Neuroscience is published by the Society for Neuroscience, an organization of nearly 38,000 basic scientists and clinicians who study the brain and nervous system.

Society for Neuroscience

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