Blocking the brain death switch in Alzheimer's slows disease in mice
Researchers at Heidelberg University and Shandong University identified a toxic interaction between NMDA receptors (NMDAR) and the TRPM4 channel that forms a 'death complex' driving neuron loss in an Alzheimer's mouse model. They used FP802 to disrupt this complex, slowing disease progression, preserving memory, reducing synaptic and mitochondrial damage, and lowering beta-amyloid buildup. This approach targets a downstream mechanism rather than amyloid, offering a potential new therapeutic path, though human trials are years away.