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Fig. 1 | Acta Neuropathologica Communications

Fig. 1

From: LATE-NC aggravates GVD-mediated necroptosis in Alzheimer’s disease

Fig. 1

The necroptosis pathway and its presumed activation in AD. Necroptosis is a programmed form of cell death which starts with the activation of death receptors. RIPK1 is then recruited and self-phosphorylated [12]. The inhibition or activation of caspase-8 determines whether necroptosis or apoptosis takes place. If caspase-8 is inhibited, the necrosome complex is formed, which includes activated pRIPK1, pRIPK3 and pMLKL. This complex translocates to the cell membrane, resulting in membrane swelling and bursting mediated by pMLKL, the necroptosis executor [12]. This is followed by release of intracellular components, inflammatory response and ultimately neuronal death. Necroptosis activation has been previously linked to AD [12]. Here, the activated necrosome components pRIPK1, pRIPK3 and pMLKL accumulate in GVD granules presumably indicating an aberrant/delayed execution process of necroptosis in neurons with GVD [41]

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