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Fig. 1 | Alzheimer's Research & Therapy

Fig. 1

From: YKL-40 changes are not detected in post-mortem brain of patients with Alzheimer’s disease and frontotemporal lobar degeneration

Fig. 1

YKL-40 immunoreactivity and protein levels remain similar in post-mortem temporal and frontal cortex from AD and non-demented controls. A Representative images of paraffin sections from temporal cortex stained with the anti-YKL-40 antibody. YKL-40 immunoreactivity is present in glial and neuronal cells in NDC and AD cases. In AD-CAA sections, YKL-40 was detected around cerebral vessels and in structures resembling amyloid plaques. Scale bars represent 50μM. Semi-quantitation of YKL-40 immunoreactivity was performed by grouping cases into negative (i.e., zero or 1 positive cell) or positive (i.e., 2 or more positive cell groups). Stacked bar plots represent the percentage of cases with either negative (−, white area) or positive (+, black area) YKL-40 immunoreactivity in NDC (n = 51), AD (n = 52), and AD-CAA cases (n = 6). Box-dot plots show quantification of YKL-40 immunoreactivity by DAB+ pixel count in NDC (n = 6, Braak stage < I, Thal stage = 0) and AD (n = 6, Braak stage > V, Thal stage = 3) cases. B Representative immunoblot of YKL-40 in frontal cortex from NDC and AD patients. Actin was used as a loading control. Box-dot plot depict YKL-40 immunoblot reactivity corrected for actin protein loading in NDC (n = 4) and AD cases (n = 5). (C) YKL-40 levels were quantified by ELISA and corrected for total protein concentration in temporal cortex (NDC = 14 and AD = 6) and frontal cortex (NDC = 4 and AD = 5). Overall, no significant differences across groups were identified. Box represents median ± interquartile range with bars showing the lowest to highest points. Abbreviations: NDC, non-demented control; AD, Alzheimer’s disease; CAA, cerebral amyloid angiopathy; n.s., non-significant difference between groups

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