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Fig. 3 | Molecular Neurodegeneration

Fig. 3

From: Decreased cortical FADD protein is associated with clinical dementia and cognitive decline in an elderly community sample

Fig. 3

Regulation of FADD (upper plots) and p-FADD (bottom plots) protein forms in the DLPFC of MAP participants ranked either by: a CERAD severity scale according to plaque pathology, and displaying no (4, n = 40), sparse (3, n = 26), moderate (2, n = 42), or frequent (1, n = 42) plaque load; b Braak staging according to the spread of the tauopathy, and displaying no or transentorhinal deposition (0–II, n = 26), limbic spread (III–IV, n = 92), or neocortical spread (V–VI, n = 32); or (c) clinical diagnoses with no cognitive impairment (NCI, n = 51), mild-cognitive impairment (NCI, n = 42) or dementia (DEM, n = 57). Whiskers represent 10th and 90th percentiles of FADD or p-FADD values (normalized by β-actin protein content), with boxed interquartile ranges crossed by the median for each experimental group and expressed as percentage of an in-gel-standard. Differences among groups were assessed (after log-transformation and standardization of the datasets) by ANCOVA controlling for age, sex, education and PMI followed by Tukey’s HSD post hoc test. **p < 0.01. d Representative immunoblots of FADD, p-FADD and β-actin, with various participants and standard (ST) samples. The molecular masses of the various proteins are indicated in kDa. Full gel images are included in Additional file 2: Figure S2

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