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Adult behavioural phenotyping confirmed dramatic changes in locomotor coordination and spatial learning, as well as memory defects of Ms5Yah mice.
Furthermore, insulin supplementation does not rescue the learning and memory defects of the disease, which are the most devastating symptoms of FAS (McGough et al., 2009), indicating the existence of other important developmental targets of ethanol.
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Selective expression of DopR + in the KCs using MB247-GAL4 significantly rescued the memory defect of the mutant.
Two explanations are possible to account for the remote memory defect of the cKO mice: a memory storage defect, or a remote memory retention and retrieval problem.
Consistent with these observations, restoring expression of the D1-like dopamine receptor specifically in the γ Kenyon cells has been shown to rescue the aversive odor memory defect of a receptor mutant (Qin et al., 2012).
Second, an artificial mutation (L17P) that decreased Aβ42 aggregation proneness suppressed the toxicities toward locomotor function and lifespan, but caused earlier onset of memory defects (Figure 2), showing that not all pathogenic effects of Aβ42 correlate directly with aggregation proneness.
Surprisingly, however, Aβ42art caused earlier onset of memory defects than Aβ42.
However, the onset of memory defects measured by Pavlovian olfactory classical conditioning [23] did not follow this simple trend.
For 10 dae flies, all Aβ flies reached a similar level of memory defects in the male group (left panel in Figure 2D).
Preclinical passive immunotherapy studies with monoclonal anti-Aβ antibodies in a mouse model of AD showed antibody binding to Aβ plaques, reduction in Aβ plaque burden, and reversal of memory defects [ 6, 7].
It has been pointed out that circumscribed damage to the mammillary bodies is not invariably associated with memory defect; cases of amnesia evidently occur in which these structures are spared.
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