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February 2021; 7 (1) Views & ReviewsOpen Access

Can Anti–β-amyloid Monoclonal Antibodies Work in Autosomal Dominant Alzheimer Disease?

View ORCID ProfileBruno P. Imbimbo, Ugo Lucca, Mark Watling
First published December 17, 2020, DOI: https://doi.org/10.1212/NXG.0000000000000535
Bruno P. Imbimbo
From the Department of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.
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  • ORCID record for Bruno P. Imbimbo
Ugo Lucca
From the Department of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.
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Mark Watling
From the Department of Research & Development (B.P.I.), Chiesi Farmaceutici, Parma, Italy; Laboratory of Geriatric Neuropsychiatry (U.L.), Department of Neuroscience, Istituto di Ricerche Farmacologiche Mario Negri IRCCS, Milano, Italy; and CNS & Pain Department (M.W.), TranScrip Partners, Reading, United Kingdom.
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Can Anti–β-amyloid Monoclonal Antibodies Work in Autosomal Dominant Alzheimer Disease?
Bruno P. Imbimbo, Ugo Lucca, Mark Watling
Neurol Genet Feb 2021, 7 (1) e535; DOI: 10.1212/NXG.0000000000000535

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    Figure Scheme of the Structural and Functional Relationships of APP

    Asterisks indicate pathogenic APP mutations that have been identified in familial AD, which cluster near the α-secretase, β-secretase (BACE1), and γ-secretase cleavage sites. AD = Alzheimer disease; APP = amyloid precursor protein; BACE1 = β-site APP cleaving enzyme-1.

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Neurology Genetics: 9 (2)

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