ArticleCell death & disease2015
Amyloid-β reduces the expression of neuronal FAIM-L, thereby shifting the inflammatory response mediated by TNFα from neuronal protection to death.
Article in Cell death & disease, 2015. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 24 papers.
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Who cites it
24 citing papers in PubMed, 40 citations in OpenAlex.
- Genetic influence of the brain on epigenetic age acceleration: evidence of a large-scale genetic correlation study.Biogerontology · 2025Article
- Cell death in glioblastoma and the central nervous system.Cellular oncology (Dordrecht, Netherlands) · 2025Review
- Ellagic acid improves the symptoms of early-onset Alzheimer's disease: Behavioral and physiological correlates.Heliyon · 2024Article
- Epigenetics in the formation of pathological aggregates in amyotrophic lateral sclerosis.Frontiers in molecular neuroscience · 2024Review
- Newfound physiological function of FAIM protein offers hope of novel disease-modifying therapy for Alzheimer's disease.Neural regeneration research · 2023Article
- Therapeutic Potential of P110 Peptide: New Insights into Treatment of Alzheimer's Disease.Life (Basel, Switzerland) · 2023Article
- Article
- Small Heat Shock Proteins Collaborate with FAIM to Prevent Accumulation of Misfolded Protein Aggregates.International journal of molecular sciences · 2022Article
- Article
- Pharmacological ablation of astrocytes reduces Aβ degradation and synaptic connectivity in an ex vivo model of Alzheimer's disease.Journal of neuroinflammation · 2021Article
- Fas Apoptosis Inhibitory Molecule Blocks and Dissolves Pathological Amyloid-β Species.Frontiers in molecular neuroscience · 2021Article
- FAIM-L - SIVA-1: Two Modulators of XIAP in Non-Apoptotic Caspase Function.Frontiers in cell and developmental biology · 2021Review
- FAIM-S functions as a negative regulator of NF-κB pathway and blocks cell cycle progression in NSCLC cells.Cell cycle (Georgetown, Tex.) · 2020Article
- SIVA-1 regulates apoptosis and synaptic function by modulating XIAP interaction with the death receptor antagonist FAIM-L.Cell death & disease · 2020Article
- Article
- FAIM: An Antagonist of Fas-Killing and Beyond.Cells · 2019Review
- Impaired Peripheral Lymphatic Function and Cerebrospinal Fluid Outflow in a Mouse Model of Alzheimer's Disease.Journal of Alzheimer's disease : JAD · 2019Article
- Physiological Aβ Concentrations Produce a More Biomimetic Representation of the Alzheimer's Disease Phenotype in iPSC Derived Human Neurons.ACS chemical neuroscience · 2018Article
- Identification and characterization of new isoforms of human fas apoptotic inhibitory molecule (FAIM).PloS one · 2017Article
- FAIM-L regulation of XIAP degradation modulates Synaptic Long-Term Depression and Axon Degeneration.Scientific reports · 2016Article
Corrections and comments
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Authors and funding
10 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
The brains of patients with Alzheimer's disease (AD) present elevated levels of tumor necrosis factor-α (TNFα), a cytokine that has a dual function in neuronal cells. On one hand, TNFα can activate neuronal apoptosis, and on the other hand, it can protect these cells against amyloid-β (Aβ) toxicity. Given the dual behavior of this molecule, there is some controversy regarding its contribution to the pathogenesis of AD. Here we examined the relevance of the long form of Fas apoptotic inhibitory molecule (FAIM) protein, FAIM-L, in regulating the dual function of TNFα. We detected that FAIM-L was reduced in the hippocampi of patients with AD. We also observed that the entorhinal and hippocampal cortex of a mouse model of AD (PS1(M146L)xAPP(751sl)) showed a reduction in this protein before the onset of neurodegeneration. Notably, cultured neurons treated with the cortical soluble fractions of these animals showed a decrease in endogenous FAIM-L, an effect that is mimicked by the treatment with Aβ-derived diffusible ligands (ADDLs). The reduction in the expression of FAIM-L is associated with the progression of the neurodegeneration by changing the inflammatory response mediated by TNFα in neurons. In this sense, we also demonstrate that the protection afforded by TNFα against Aβ toxicity ceases when endogenous FAIM-L is reduced by short hairpin RNA (shRNA) or by treatment with ADDLs. All together, these results support the notion that levels of FAIM-L contribute to determine the protective or deleterious effect of TNFα in neuronal cells.
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