Losing the activity of a key ion channel in the brain may contribute to the buildup of a devastating and toxic protein responsible for the clumps of plaque that accumulate in Alzheimer's disease, a team of neurobiologists in China has found.
. The ion channel, therefore, helps shape critical cellular activities, such as excitability, plasticity and metabolism.. As difficult as it may be to imagine, this complex constituent in the neuronal membrane is also an enzyme—a kinase—that catalyzes the transfer of high-energy phosphate groups from potent ATP molecules to fuel activities involving TRPM7.
The Shanghai scientists not only revealed in their research that TRPM7 declines in Alzheimer's disease, the team also conducted a series of experiments with mouse models and showed that diminished amounts of TRPM7 in cell membranes resulted in the accumulation of amyloid-β. Then, in younger animals the kinase portion alone was introduced and overexpressed. And when M7CK was tested in this cohort, the kinase directly activated a cascade of activities. For example, the protease, MMP14, promoted amyloid-β degradation and clearance. The kinase actually helped sweep destructive amyloid-β out of the brains of these animals.
are a cause of the disease. Although clearly toxic to the brain, the plaque formations may occur in the aftermath of a subtler series of deleterious events that have yet to be discovered.
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