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Fig. 1 | Molecular Neurodegeneration

Fig. 1

From: Gad67 haploinsufficiency reduces amyloid pathology and rescues olfactory memory deficits in a mouse model of Alzheimer’s disease

Fig. 1

Characterization of the GAD67-GFP knock-in transgenic mice. a Most GABA immunopositive cells (red) are also GFP positive (green) in both frontal cortex (FCX) and dentate gyrus (DG) in hippocampus of the adult GAD67-GFP knock-in mice. b In frontal cortex and dentate gyrus of hippocampus, all of the parvalbumin (PV) positive cells (one subtype of GABAergic neurons) (red) are labeled by GFP (green). c Representative confocal micrographs display the expression level of GAD67 (red) in GAD67-GFP knock-in mice and GFP-negative mice of 10–11 months old. Dotted line circled regions were zoomed in and were shown in the lower left corner of each micrograph. Quantification data showing GAD67 intensity in frontal cortex (FCX), CA1, CA3, dentate gyrus (DG) and olfactory bulb (OB) of GAD67-GFP knock-in mice is significantly reduced to about half of the GAD67 content level in WT controls. For a-c, scale bars represent 30 μm. N = 5 WT mice and 5 GAD67-GFP knock-in mice. Data are presented as mean ± s.e.m., * < 0.05; ** < 0.01; *** < 0.001; Student’s t-test

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