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In this study, to test this hypothesis of non-cell autonomous effects by glial cells as well as by stem/progenitor cells, we generated and analyzed phenotypes of Drosophila models expressing human mutant Htt or Atx1 in the glial cell lineage at different stages of differentiation.
Drosophila models expressing human Ataxin-3 proteins have provided novel insights into SCA3 disease (10– 10).
The apoE isoforms strongly influence amyloid deposition in the human brain (apoE4 > noncarriers) and in amyloid precursor protein (APP) mouse models expressing human apoE isoforms (apoE4 > apoE3 > apoE2).
Elevated p38 activity is found in brains from patients with tauopathies (145– 147) and in transgenic AD mice models expressing human tau (148– 150) or mutant APP (151), both of which correlate with tau aggregation.
E-64d treatment rescued memory function, and decreased brain A β1-42/amyloid and amyloid plaque neuropathology in AD animal models expressing human APP containing the wild-type β- and London mutant γ-secretase site (APPLon) sequences 171, 177.
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To clarify the role of adipocyte-derived SAA, a transgenic mouse model expressing human SAA1 (hSAA) in adipocytes was established.
An AD mouse model expressing human amyloid precursor protein (hAPP) with Swedish and Indiana mutations [ 55].
Our report identified several autophagy genes as strong modifiers of neurodegeneration using an in vivo model expressing human MAPT in Drosophila.
P McLaughlin (Groningen, the Netherlands) investigated the consequences of targeting monoclonal antibodies to normal and tumour tissue in a transgenic murine model expressing human EpCAM.
Here we followed the fate of single dendritic spines in the neocortex of a tauopathy mouse model, expressing human P301S mutated tau, for a period of two weeks.
Recently, a transgenic mouse model expressing human APP with the 714 austrian mutation has been reported showing intraneuronal Aβ accumulation correlating with brain atrophy [ 65].
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Justyna Jupowicz-Kozak
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