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In fact, adult hippocampal neurogenesis appears to be necessary for hippocampus-dependent learning and memory, as indicated by severe cognitive deficits following ablation of neurogenesis in mice models by toxins, x-ray irradiation or virus-activated pro-drugs [19], [20], [21].
As showed in Fig. 2, forgetting can be observed in the Fear rats: without any extinction training, these rats can establish some extinction memory as indicated by the gradually decreased freezing score which was significant on R 3 d (P<0.05, vs. F).
Rats treated with 0.25 mg.Kg−1 vitexin, isovitexin (0.1 or 0.25 mg.Kg−1) and 6-C-glycoside-diosmetin and FfA or FfB exhibited enhanced retention of fear memory, as indicated in T1 to T3.
Indeed, eIF2α phosphorylation also plays a role in dynamic restructuring of memory, as indicated by studies showing that ablation of PERK in the brain impairs behavioral flexibility (Trinh et al., 2012).
Importantly, the cognitive impairment was selective to the domain of memory, as indicated by their achievement of average-range scores on tests of intelligence, academic attainments, and verbal fluency.
The newborn schedule of 7vPCV was immunogenic at 18 weeks and induced immunological memory, as indicated by brisk booster responses at 36 weeks, with no evidence of immunological tolerance.
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Our goal was to test the hypothesis that the PPC would be involved in the recollection of episodic memories, as indicated by greater activation for hits compared with CRs of unrelated lures.
Healthy control participants appear to recruit different neural networks for maintaining items in verbal WM in true memory compared with false memory trials as indicated by deactivated prefrontal regions in true memory.
As expected, compared to control (PS1KI) animals [30], 3xTg-AD mice showed no impairment in short-term memory while they manifested long-term memory deficits as indicated by the statistically significant increase in the time spent to find the platform (Figure 2).
As previously reported, 3xTg-AD mice displayed no impairment in short-term memory, while they manifested long-term memory deficits as indicated by the statistically significant increase in the time spent to find the platform (control versus 3xTg-AD; (P=0.010)).
Our eight-arm radial maze memory test also revealed a steady age-dependent decline in learning and memory functions as indicated by the decreasing percentage of mice that passed this cognitive test with increasing age (summarized in Table 1), which confirms that there exists a functional correlation between genomic DNA methylation levels and cognitive performance during the aging process.
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