Early Phenotypic Changes in Transgenic Mice That Overexpress Different Mutants of Amyloid Precursor Protein in Brain
Dieder Moechars(Janssen (Belgium)), Fred Van Leuven(KU Leuven), Barbara Cordell(Unknown), Chris Van den Haute(Neuroelectronics Research Flanders), Emile Godaux(University of Mons), Kurt Spittaels(Vlaams Instituut voor Biotechnologie), Ilse Dewachter(Hasselt University), Ina Tesseur(Stanford University), Veerle Baekelandt(Allen Institute for Brain Science), Frédéric Checler(Centre National de la Recherche Scientifique), Kristin Lorent(Vlaams Instituut voor Biotechnologie), Asha Naidu, Delphine Reversé(University of Mons)
Cited by 668
Related Papers
Hallmarks of neurodegenerative diseases
|Cell|2023|1.6k
Association of Amyloid and Tau With Cognition in Preclinical Alzheimer Disease
|JAMA Neurology|2019|876
A disintegrin-metalloproteinase prevents amyloid plaque formation and hippocampal defects in an Alzheimer disease mouse model
|Journal of Clinical Investigation|2004|622
Presenilin 2 deficiency causes a mild pulmonary phenotype and no changes in amyloid precursor protein processing but enhances the embryonic lethal phenotype of presenilin 1 deficiency
|Proceedings of the National Academy of Sciences|1999|523