T
Takahisa Kanekiyo
Researcher at Mayo Clinic
Publications - 107
Citations - 9158
Takahisa Kanekiyo is an academic researcher from Mayo Clinic. The author has contributed to research in topics: Apolipoprotein E & LRP1. The author has an hindex of 40, co-authored 91 publications receiving 6691 citations. Previous affiliations of Takahisa Kanekiyo include Osaka University & Osaka Bioscience Institute.
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Journal ArticleDOI
Apolipoprotein E and Alzheimer disease: risk, mechanisms and therapy
TL;DR: The A β-dependent and Aβ-independent mechanisms that link Apo-E4 status with AD risk are discussed, and how to design effective strategies for AD therapy by targeting ApO-E is considered.
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ApoE and Aβ in Alzheimer's disease: accidental encounters or partners?
TL;DR: Among the three human apolipoprotein E (apoE) isoforms, apoE4 increased the risk of Alzheimer's disease as mentioned in this paper, while transporting cholesterol is a primary function, apioE also regulates amyloid-β (Aβ) metabolism, aggregation, and deposition.
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Central role for PICALM in amyloid-β blood-brain barrier transcytosis and clearance
Zhen Zhao,Abhay P. Sagare,Qingyi Ma,Matthew R. Halliday,Pan Kong,Kassandra Kisler,Ethan A. Winkler,Anita Ramanathan,Takahisa Kanekiyo,Guojun Bu,Nelly Chuqui Owens,Sanket V Rege,Gabriel Si,Ashim Ahuja,Donghui Zhu,Carol A. Miller,Julie A. Schneider,Manami Maeda,Takahiro Maeda,Takahiro Maeda,Tohru Sugawara,Justin K. Ichida,Berislav V. Zlokovic +22 more
TL;DR: PICALM regulated PICALM/clathrin-dependent internalization of Aβ bound to the low density lipoprotein receptor related protein-1, a key Aβ clearance receptor, and guided Aβ trafficking to Rab5 and Rab11, leading to Aβ endothelial transcytosis and clearance.
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Blood-Brain Barrier Dysfunction and the Pathogenesis of Alzheimer's Disease.
Yu Yamazaki,Takahisa Kanekiyo +1 more
TL;DR: Current evidence suggests that BBB dysfunction may causatively and consequently contribute to AD pathogenesis, forming a vicious cycle between brain Aβ accumulation and neurovascular unit impairments during disease progression.
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APOE4-specific Changes in Aβ Accumulation in a New Transgenic Mouse Model of Alzheimer Disease
Katherine L. Youmans,Leon M. Tai,Evelyn Nwabuisi-Heath,Lisa Jungbauer,Takahisa Kanekiyo,Ming Gan,Jungsu Kim,William A. Eimer,Steve Estus,G. William Rebeck,Edwin J. Weeber,Guojun Bu,Chunjiang Yu,Mary Jo LaDu +13 more
TL;DR: APOE differentially regulates multiple aspects of Aβ accumulation, and its effects on plaque morphology, intraneuronal Aβ, soluble Aβ42, and oligomeric Aβ (oAβ) are determined using new EFAD transgenic mice.