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Overall these data support our hypothesis that amygdalar CRF is critical in anxiety-like behavior; because the antidepressant was unable to reverse behavioral manifestations of CeA CRF-OE.
This study showed a better survival rate with IgM-enriched immunoglobulin administration during sepsis; however, both immunoglobulin preparations were able to reverse behavioral deficits within 10 days, which were resolved by 60 days after surgery in all groups.
Both active and passive immunization strategies have been demonstrated to significantly reduce the amount of Aβ plaques and the associated neuritic dystrophy within the brain as well as reverse behavioral deficits in animal models of disease.
Given the accelerated investments in mouse genetics and behavior, experimenters need to be aware that the early environment, such as housing condition, can eliminate or even reverse behavioral differences ascribed to genetics (e.g., Crabbe 1999).
This hypothesis is consistent with recent study which showed that FTY720, an agonist of S1P receptors with high affinity for S1P1 was able to reverse behavioral impairment in rat model of AD [ 40].
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However, both immunoglobulin preparations were equally effective in reversing behavioral deficits induced by sepsis [12].
Both diets reversed behavioral impairments and inhibited the mTOR activity in the prefrontal cortex and amygdala of CMA mice.
In contrast to clinical trials utilizing monotherapies, combinations of dopamine (DA) agonists and selective 5-HT3, 5HT2A/2C, or NK1 antagonists have shown robust efficacy in reversing behavioral and neurobiological alterations in animal models of psychostimulant abuse.
Preclinical studies demonstrated that treatement with atomoxetine plus lDOPS, a synthetic precursor in norepinephrine biosynthesis, increased norepinephrine, nerve growth factor brain-derived neurotrophic factor levels, decreased amyloid plaque load, and reversed behavioral deficits in the 5xFAD model.
This program resulted in the development of MW151, a highly selective, BBB penetrable compound that effectively attenuated pro-inflammatory cytokine production and reversed behavioral deficits following oral administration in an amyloid-β-induced brain injury mouse model.
While the manuscript of this review was in the review process, Sehgal et al. (Proc Natl Acad Sci U S A 2012, 109 3510-3515) reported that oral administration of a semipurified extract of the Ashwagandha (W. somnifera) root reversed behavioral deficits, plaque load, and accumulation of beta-amyloid peptides in mouse models of AD.
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