ArticleMolecular neurodegeneration2017
Decreased cortical FADD protein is associated with clinical dementia and cognitive decline in an elderly community sample.
Article in Molecular neurodegeneration, 2017. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 13 papers.
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Who cites it
13 citing papers in PubMed, 24 citations in OpenAlex.
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- Synaptic Function and Dysfunction in Lysosomal Storage Diseases.Frontiers in cellular neuroscience · 2021Article
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- Increased inflammation in BA21 brain tissue from African Americans with Alzheimer's disease.Metabolic brain disease · 2020Article
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- A Cell's Fate: An Overview of the Molecular Biology and Genetics of Apoptosis.International journal of molecular sciences · 2019Review
- Behavioral and Cognitive Improvement Induced by Novel Imidazoline INeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics · 2019Article
- Religious Orders Study and Rush Memory and Aging Project.Journal of Alzheimer's disease : JAD · 2018Review
- Trigeminal neuralgia causes neurodegeneration in rats associated with upregulation of the CD95/CD95L pathway.Molecular painArticle
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Authors and funding
10 authors at 5 institutions in 4 countries.
Funding
Abstract
backgroundFADD (Fas-associated death domain) adaptor is a crucial protein involved in the induction of cell death but also mediates non-apoptotic actions via a phosphorylated form (p-Ser194-FADD). This study investigated the possible association of FADD forms with age-related neuropathologies, cognitive function, and the odds of dementia in an elderly community sample.
methodsFADD forms were quantified by western blot analysis in dorsolateral prefrontal cortex (DLPFC) samples from a large cohort of participants in a community-based aging study (Memory and Aging Project, MAP), experiencing no-(NCI, n = 51) or mild-(MCI, n = 42) cognitive impairment, or dementia (n = 57).
resultsCortical FADD was lower in subjects with dementia and lower FADD was associated with a greater load of amyloid-β pathology, fewer presynaptic terminal markers, poorer cognitive function and increased odds of dementia. Together with the observations of FADD redistribution into tangles and dystrophic neurites within plaques in Alzheimer's disease brains, and its reduction in APP23 mouse cortex, the results suggest this multifunctional protein might participate in the mechanisms linking amyloid and tau pathologies during the course of the illness.
conclusionsThe present data suggests FADD as a putative biomarker for pathological processes associated with the course of clinical dementia.
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