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In addition, there is a strong circadian rhythm in nucleotide excision repair activity in the mouse brain, caused at least partly by circadian regulation of xeroderma pigmentosum A (XPA) [ 23].
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Autophagy may be involved in this process because autophagy is impaired in AD and lack of autophagy in the mouse brain causes neurodegeneration [ 33, 34].
His group successfully experimented with in situ tissue engineering using a combination of injectable and biodegradable scaffolds and hESC-derived neural stem cells to mouse brain cavity caused by experimental stroke.
However, consistent with other in vivo efficacy studies [ 37], a dodecameric soluble Aβ oligomer extracted from aged Tg2576 mouse brain (Aβ*56) caused significant cognitive deficits.
The procedure resulted in a stable depletion of both neurotransmitters (ACh and DA) in the mouse brain without causing gross motor deficits.
WP supplementation improves the behavior of diabetic mice and reduces neuronal damage in the brain caused by oxidative stress.
Examination of mouse embryos showed that Cre-mediated recombination in the developing brain caused an increase in cell death.
As PS1 mutations causing early-onset AD modulate protein expression by disrupting endoplasmic reticulum homeostasis, to determine whether decreased Crif1 levels in Tg6799 and APP/PS1 mouse brains were caused by PS1 mutations, we measured Crif1 levels in the brains of 12-month-old Tg2576 mice that carry only the APP mutation (Supplementary Figure 1c).
Since telomerase protects mitochondria and cells from oxidative stress (Haendeler et al, 2009), it is possible that AGS-499 that increases telomerase in neurons may protects the motor neurons (and/or other cells) in the mouse brain from degeneration caused by oxidative damage.
Deletion of claudin 5 in mice showed detrimental effects on the brain causing early death; those effects were due to a size-selective loosening of the BBB for molecules with MW<800 Da [ 23].
Previous experiments show that Al overload caused mouse brain damage and an increased expression of cyclooxygenase2 (COX2) [ 17].
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