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(C) Lack of plaque detection in a wild-type mouse following SPION-Aβ(1 42) injection (from [30], with permission).
Our study provides an alternative explanation for the lack of side effects: the lack of plaque engagement by the antibody.
Clinical strains may exit the cell without cellular disruption, facilitating subsequent rounds of infection and lack of plaque formation.
Lack of plaque growth is supported by a similar finding in aged Tg2576 mice, another mouse model of AD [ 8, 9].
Considering the large synaptic changes seen in 2-month-old TASTPM mice in the CA1 region, despite the lack of plaque deposition, one possibility was that the effects seen were developmental, due to the position of transgene insertion or overexpression of the APP and/or PSEN1, independent of increasing amyloid-β levels.
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Lack of amyloid plaque deposition at 3 months.
The lack of classic plaque formation for clinical isolates likely stems from their slow growth and lack of adaptation to conventional cell culture.
Nevertheless we think that the results of our study are interesting and worth to be presented despite the lack of systematic plaque assessment because there are very few studies published who examined the association of reproductive parameters and CP.
If scans show a lack of amyloid plaques, the "worried well" could be reassured that they don't have Alzheimer's and doctors could pursue other lines of medical inquiry, like investigating the potential for thyroid problems, depression or vitamin B12 deficiency, said Dr. Paul Aisen, a professor of neuroscience at the University of California, San Diego, School of Medicine.
Pharmacokinetics data in normal mice indicate a higher initial influx into the brain, followed by clearance due to a lack of targeted plaques within the brains of normal mice, an important factor that could determine critical target/background ratios.
It has been hypothesized that the phenotype with kuru plaques in p-dCJD is caused by a cross-sequence transmission of sCJDMV2 or sCJDVV2 prions to dura mater recipients with 129MM genotype, whereas the lack of kuru plaques in np-dCJD would be explained by an infection with prions from sCJDMM1 [ 33, 43, 44].
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