Connexin43 hemichannel-blocking peptide restores cognition in Alzheimer's mouse model
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Researchers showed that connexin43 hemichannels open abnormally on reactive astrocytes and microglia surrounding amyloid plaques in Alzheimer's brains and APP/PS1 mice, driving calcium influx and ATP and glutamate release that harms neurons. Working with Aha, they delivered a TAT-Cx43 peptide in VPN lipid nanoparticles, achieving seven-day brain exposure after intraperitoneal injection and selectively blocking hemichannels while sparing gap junctions. In APP/PS1 mice, weekly dosing — either from 8 months for seven weeks or from 3.5 months for nine weeks — improved cognition, cut oxidative stress and dendritic spine loss, and shifted microglia toward a neuroprotective state. The work is at the preclinical stage; whether the approach translates to human Alzheimer's disease is unresolved.
Written by a model from the reports · updated 2 hours ago
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Researchers found that connexin43 hemichannels open abnormally on reactive astrocytes and microglia near amyloid plaques in Alzheimer's disease brains and APP/PS1 mice, mediating calcium influx and ATP/glutamate release that damage neurons. In collaboration with Aha, they used a TAT-Cx43 peptide, delivered in VPN lipid nanoparticles giving seven-day brain exposure after intraperitoneal injection, to selectively block hemichannels while sparing gap junctions. In APP/PS1 mice, weekly dosing either from 8 months for seven weeks or from 3.5 months for nine weeks improved cognition, reduced oxidative stress and dendritic spine loss, and shifted microglia toward a neuroprotective state.
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