"Researchers have unveiled the mystery behind neuron death in Alzheimer’s disease. A groundbreaking study reveals that neurons undergo a programmed cell death, necroptosis, when exposed to amyloid plaques and tau tangles, hallmark proteins linked to Alzheimer’s. The study pinpoints an RNA gene called MEG3 as a potential key player in this process. This pivotal discovery provides promising pathways for future treatments."
"More importantly, the research team was able to prevent the death of neurons, rescuing them in the process. The discovery opens new pathways for potential future treatments."
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Written by
PDWarrior1900
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MEG3 activates necroptosis in human neuron xenografts modeling Alzheimer’s disease
Neuronal cell loss is a defining feature of Alzheimer’s disease (AD), but the underlying mechanisms remain unclear. We xenografted human or mouse neurons into the brain of a mouse model of AD.
Only human neurons displayed tangles, Gallyas silver staining, granulovacuolar neurodegeneration (GVD), phosphorylated tau blood biomarkers, and considerable neuronal cell loss.
The long noncoding RNA MEG3 was strongly up-regulated in human neurons. This neuron-specific long noncoding RNA is also up-regulated in AD patients. MEG3 expression alone was sufficient to induce necroptosis in human neurons in vitro.
Down-regulation of MEG3 and inhibition of necroptosis using pharmacological or genetic manipulation of receptor-interacting protein kinase 1 (RIPK1), RIPK3, or mixed lineage kinase domain-like protein (MLKL) rescued neuronal cell loss in xenografted human neurons.
This model suggests potential therapeutic approaches for AD and reveals a human-specific vulnerability to AD."
"More importantly, the research team was able to prevent the death of neurons, rescuing them in the process. The discovery opens new pathways for potential future treatments."
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