BACE1 gene deletion: Impact on behavioral function in a model of Alzheimer’s disease

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Untitled work

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Behavioral disturbances in transgenic mice overexpressing the V717F Β-amyloid precursor protein.

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The β-Secretase BACE1 in Alzheimer’s Disease

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Alzheimer's disease as homeostatic responses to age-related myelin breakdown

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The Alzheimer’s β-secretase BACE1 localizes to normal presynaptic terminals and to dystrophic presynaptic terminals surrounding amyloid plaques

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BACE1 Deficiency Causes Altered Neuronal Activity and Neurodegeneration

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Seizure protein 6 and its homolog seizure 6-like protein are physiological substrates of BACE1 in neurons

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Modulation of γ- and β-secretases as early prevention against Alzheimer's disease

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Aging Increased Amyloid Peptide and Caused Amyloid Plaques in Brain of Old APP/V717I Transgenic Mice by a Different Mechanism than Mutant Presenilin1

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