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At P40, double BrdU- and GFAP-immunolabeled cells were very scarce both in the neocortex and hippocampus (Fig. 3 K,L ).
Quantitative analysis of amyloid burden (Fig. 4 E,F) showed a significant lithium treatment effect in the total Aβ plaque area, in the plaque number and in the minimum and maximum plaque areas, both in the neocortex and hippocampus.
IBA-1 antibody showed microglial cells with small cell bodies and thin and elongated processes, both in the neocortex and hippocampus, in the lithium-treated Tg (Fig. 6 B,D), compared to saline-treated Tg mice (Fig. 6 A,C), where microglial cells with enlarged cell bodies and short and thickened processes were found.
Together this demonstrates that a number of genes associated with ASD are coordinately expressed across postnatal development, both in the neocortex and the striatum.
Overall, there were statistically significant differences in the patterns of COX immunoreactivity between the different experimental groups, both in the neocortex and the hippocampus (both P < 0.0001; Figure 5).
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Despite the broad expression of both proteins in the neocortex, it is not possible to verify that all of the analyzed neurons did express the tau transgene.
Relative to WT mice, the COX labelling intensity and area were reduced in K3 mice in both the neocortex and the hippocampus (>70% and >75% reductions, respectively).
Mezey et al. [ 28] in 2003 showed in four patients tested (survival between 2 and 10 months post-transplant) that BM cells contributed to neuronal populations in the CNS, particularly in both the neocortex and hippocampal regions.
In humans, neocortical GABAergic interneurons are derived from Dlx-expressing populations in both the neocortex and the ganglionic eminences (GE) [40], whilst those of the thalamus are derived from the GE; a migratory pathway not found in rodents [41].
Immunohistochemical labelling with the anti-Aβ antibody 4G8 revealed a significant reduction in percentage plaque burden, average plaque size and number of plaques in both the neocortex and the hippocampus of NIr-treated APP/PS1 mice relative to untreated APP/PS1 controls.
Synaptic loss in both the neocortex and the hippocampus is, so far, the best pathological correlate of early cognitive decline [ 19, 41, 52– 59, 59, 61].
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