NDLI: BACE1 Elevation is Involved in Amyloid Plaque Development in the Triple Transgenic Model of Alzheimer’s Disease: Differential Aβ Antibody Labeling of Early-Onset Axon Terminal Pathology

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BACE1 Elevation is Involved in Amyloid Plaque Development in the Triple Transgenic Model of Alzheimer’s Disease: Differential Aβ Antibody Labeling of Early-Onset Axon Terminal Pathology

Content Provider	Springer Nature Link
Author	Cai, Yan Zhang, Xue Mei Macklin, Lauren N. Cai, Huaibin Luo, Xue Gang Oddo, Salvatore LaFerla, Frank M. Struble, Robert G. Rose, Gregory M. Patrylo, Peter R. Yan, Xiao Xin
Copyright Year	2011
Abstract	β-amyloid precursor protein (APP) and presenilins mutations cause early-onset familial Alzheimer’s disease (FAD). Some FAD-based mouse models produce amyloid plaques, others do not. β-Amyloid (Aβ) deposition can manifest as compact and diffuse plaques; it is unclear why the same Aβ molecules aggregate in different patterns. Is there a basic cellular process governing Aβ plaque pathogenesis? We showed in some FAD mouse models that compact plaque formation is associated with a progressive axonal pathology inherent with increased expression of β-secretase (BACE1), the enzyme initiating the amyloidogenic processing of APP. A monoclonal Aβ antibody, 3D6, visualized distinct axon terminal labeling before plaque onset. The present study was set to understand BACE1 and axonal changes relative to diffuse plaque development and to further characterize the novel axonal Aβ antibody immunoreactivity (IR), using triple transgenic AD (3xTg-AD) mice as experimental model. Diffuse-like plaques existed in the forebrain in aged transgenics and were regionally associated with increased BACE1 labeled swollen/sprouting axon terminals. Increased BACE1/3D6 IR at axon terminals occurred in young animals before plaque onset. These axonal elements were also co-labeled by other antibodies targeting the N-terminal and mid-region of Aβ domain and the C-terminal of APP, but not co-labeled by antibodies against the Aβ C-terminal and APP N-terminal. The results suggest that amyloidogenic axonal pathology precedes diffuse plaque formation in the 3xTg-AD mice, and that the early-onset axonal Aβ antibody IR in transgenic models of AD might relate to a cross-reactivity of putative APP β-carboxyl terminal fragments.
Starting Page	160
Ending Page	174
Page Count	15
File Format	PDF
ISSN	10298428
Journal	Neurotoxicity Research
Volume Number	21
Issue Number	2
e-ISSN	14763524
Language	English
Publisher	Springer-Verlag
Publisher Date	2011-07-02
Publisher Place	New York
Access Restriction	One Nation One Subscription (ONOS)
Subject Keyword	Amyloid plaque Axonal pathology Synaptoplasticity Aging Dementia Neurochemistry Neurobiology Pharmacology/Toxicology Neurology Neurosciences Cell Biology
Content Type	Text
Resource Type	Article
Subject	Neuroscience Toxicology

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BACE1 Elevation is Involved in Amyloid Plaque Development in the Triple Transgenic Model of Alzheimer’s Disease: Differential Aβ Antibody Labeling of Early-Onset Axon Terminal Pathology