A new cellular mechanism linked to neuronal damage during stroke is reported this week in Nature Medicine. Targeting this mechanism may have therapeutic potential in people.
Damage caused by overactivation of excitatory receptors in the brain is a principal cause of neuronal loss after stroke. Among these receptors, the so-called NMDA subtype of glutamate receptors is a key player. Yu Tian Wang and his team found that activation of a molecule called SREBP-1 in affected neurons is an essential step in NMDA receptor-mediated neuronal death in stroke in mice.
According to the authors, the activation of SREBP-1 is linked to the loss of a known SREBP-1 binding partner known as Insig-1. Using a compound capable of inhibiting the loss of Insig-1, the team could interfere with SREBP-1 activation, and therefore reduce neuronal damage and prevent neurological deficits after stroke in mice. This highlights the potential of agents that reduce SREBP-1 activation in cases of stroke.
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