Affiliations: Center for Neurologic Diseases, Department of Neurology, Brigham and Women's Hospital and Harvard Medical School, Boston, MA, USA
Correspondence:
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Correspondence to: Weiming Xia, Ph.D., Center for Neurologic Diseases, Harvard Institute of Medicine, HIM 616, 77 Avenue Louis Pasteur, Boston, MA 02115, USA. Tel.: +1 617 525 5212; Fax: +1 617 525 5252; E-mail: [email protected].
Note: [] Handling Associate Editor: Xiongwei Zhu
Abstract: The amyloid-β protein (Aβ)-containing neuritic plaques and hyperphosphorylated tau-containing neurofibrillary tangles are two invariable characteristics of Alzheimer's disease (AD). Three genes encoding amyloid-β protein precursor (AβPP), presenilin (PS) 1 and 2 are linked to early onset familial AD, and the apolipoprotein E (ApoE) ε4 allele is a major risk factor for sporadic AD. The zebrafish AβPP, PS, and ApoE genes have been identified, and the essential components of the γ-secretase complex that mediates cleavage of AβPP to generate Aβ have been examined in zebrafish. A transgenic zebrafish expressing mutant tau has been created, and the transgenic animals exhibit a neurodegeneration phenotype. The use of zebrafish as a model system for AD research has expanded our knowledge of Aβ and tau.
