Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer's disease
Abstract
Neuronal necroptosis–an emerging form of regulated cell death associated with neuroinflammatory signaling: Alzheimer ’s disease (AD) is characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles as well as progressive neuronal loss. Recent evidence has suggested that prolonged neuroinflammation with increased levels of cytokines, arising from neuronal injury, innate immune responses from glial cells, and peripheral inflammation, leads to neuronal death and AD progression. Neuronal necroptosis is an emerging form of regulated cell death associated with neuroinflammatory signaling. Necroptosis typically occurs in response to sustained inflammation while apoptosis facilitates normal turnover of cellular contents important for growth and development. By combining features of apoptosis and necrosis, necroptosis has been proposed to constitute a more comprehensive mechanistic explanation for neurodegeneration, which is less likely to occur by the immunologically silent apoptotic cell death or by the acute occurrence of necrosis after cellular stress (Jayaraman and Reynolds, 2022).
Related
- Brain white matter functional alterations in patients with Alzheimer's disease and amnestic mild cognitive impairment.
- Carbonic anhydrase inhibition rescues heart function in the Tg2576 Alzheimer's mouse model by ameliorating cardiac amyloid-β pathology and neurotrophic signaling impairment.
- M6A demethylation of IRF9 by ALKBH5 promotes intervertebral disc degeneration via nucleus pulposus cell necroptosis
- Effect of Esketamine Pretreatment on Necroptosis in Mice with Trigeminal Neuralgia and Anxiety-Like Behavior via the RIP1/RIP3/MLKL Pathway
- Elevated procoagulant platelets driven by necroptosis and pyroptosis aggravate pulmonary thrombosis via suppressing monocyte efferocytosis in severe pneumonia
BibTeX
@article{asimakidou2026autolysosomal,
title = {{Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer's disease}},
author = {Evridiki Asimakidou and Richard Reynolds and Anna M. Barron and Chih Hung Lo},
journal = {Neural Regeneration Research},
year = {2026},
month = oct,
doi = {10.4103/1673-5374.390979},
url = {https://hal.science/hal-05777689v1},
note = {CC BY-NC-SA},
}
RIS
TY - JOUR
TI - Autolysosomal acidification impairment as a mediator for TNFR1 induced neuronal necroptosis in Alzheimer's disease
AU - Evridiki Asimakidou
AU - Richard Reynolds
AU - Anna M. Barron
AU - Chih Hung Lo
PY - 2026
DA - 2026/10/05
JO - Neural Regeneration Research
DO - 10.4103/1673-5374.390979
UR - https://hal.science/hal-05777689v1
AB - Neuronal necroptosis–an emerging form of regulated cell death associated with neuroinflammatory signaling: Alzheimer ’s disease (AD) is characterized by the presence of extracellular amyloid-β (Aβ) plaques and intracellular tau neurofibrillary tangles as well as progressive neuronal loss. Recent evidence has suggested that prolonged neuroinflammation with increased levels of cytokines, arising from neuronal injury, innate immune responses from glial cells, and peripheral inflammation, leads to neuronal death and AD progression. Neuronal necroptosis is an emerging form of regulated cell death associated with neuroinflammatory signaling. Necroptosis typically occurs in response to sustained inflammation while apoptosis facilitates normal turnover of cellular contents important for growth and development. By combining features of apoptosis and necrosis, necroptosis has been proposed to constitute a more comprehensive mechanistic explanation for neurodegeneration, which is less likely to occur by the immunologically silent apoptotic cell death or by the acute occurrence of necrosis after cellular stress (Jayaraman and Reynolds, 2022).
SN - 1673-5374
ER -