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Fig. 2 | Translational Neurodegeneration

Fig. 2

From: Parvalbumin neuroplasticity compensates for somatostatin impairment, maintaining cognitive function in Alzheimer’s disease

Fig. 2

Resilience of GABAergic interneurons in TgF344-AD rats at 12 months of age. We probed neurons within the hippocampal molecular layers to determine if this population underlies the neuronal changes in TgF344-AD rats at 9, 12, and 15 months of age (n = 8–9 rats/genotype at each age). a Tg rats exhibited a significant overall genotype-related increase (P = 0.02) in non-cell layer NeuN+ neurons. To phenotype these cells, hippocampal GABAergic interneurons were assessed by GAD67 staining. b and c Representative hippocampal GAD67 staining in 12-month NTg and Tg rats demonstrates increased interneurons primarily in Tg hilus and molecular layers of CA1 and DG. Quantification of total hippocampal (d) and molecular-layer (e) GABAergic interneurons determined a significant increase in 12-month Tgs. f A large deficit was detected in hilar GABAergic interneurons in 9- and 15-month Tgs, but not at 12 months. g There were no significant genotype differences in GAD67 neurons in the granular cell layer (GCL). h Tg rats exhibited an overall significant loss of total EC GABAergic interneurons (P = 0.01) in the entorhinal cortex (EC), compared to NTgs. i Finally, there was no genotype-related loss of EC layer II GABAergic interneurons. Scale bar, 100 μm. Data are mean ± SEM; two-way ANOVA with correction for multiple comparisons with a Holm-Sidak post hoc test (see Table 2 for complete statistics); **P < 0.01, ***P < 0.001

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