Table 2 Necroptosis in neurodegenerative diseases

Alzheimer's disease

Nec-1 improved neurobehavior in Al-treated mice model and increased survival of Al-induced neural cell death.

Nec-1 alleviated cognitive impairment with reduction of Aβ and tau abnormalities in APP/PS1 mice model.

Parkinson disease

Nec-1 ameliorated 6-OHDA treated PC12 cells survival.

Amyotrophic lateral sclerosis

Nec-1, NSA and RIP3 knockdown improved neuron viability in ALS astrocyte hES-MNs coculture system.

Increased expression of RIP1, RIP3 and MLKL in OPTN^−/− mice, post-mortem patient spinal cords.

Mutantion of RIP1 and RIP3 in OPTN^−/− mice increased neuron viability.

Huntington disease

Nec-1 increased ST14A 8plx celll survival.

Nec-1 improved R6/2 mice behavior and delayed symptom onset.

Niemann-Pick disease

Nec-1 prolong cell viability in NPC1 fibroblasts and NPC1 iPS-derived neuron.

Nec-1 delayed cerebellar Purkinje cell loss, significantly prolonged lifespan.

Increased levels of RIP1, RIP3 and MLKL in NPC1^−/− mice and post-mortem patient tissues.

Gaucher’s disease

level of RIP1, RIP3, and c-FlipS were markedly elevated in Gba^flox/flox; nestin-Cre mice.

Lifespan significantly extended in RIP3^−/− mice injected with CBE than widetype mice.