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Mustafa Janabi
Researcher at Lawrence Berkeley National Laboratory
Publications - 38
Citations - 4689
Mustafa Janabi is an academic researcher from Lawrence Berkeley National Laboratory. The author has contributed to research in topics: Dementia & Alzheimer's disease. The author has an hindex of 20, co-authored 37 publications receiving 3367 citations. Previous affiliations of Mustafa Janabi include University of California, San Francisco.
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Journal ArticleDOI
PET Imaging of Tau Deposition in the Aging Human Brain
Michael Schöll,Michael Schöll,Samuel N. Lockhart,Daniel R. Schonhaut,James P. O'Neil,Mustafa Janabi,Rik Ossenkoppele,Rik Ossenkoppele,Rik Ossenkoppele,Suzanne L. Baker,Jacob W. Vogel,Jamie Faria,Henry Schwimmer,Gil D. Rabinovici,Gil D. Rabinovici,Gil D. Rabinovici,William J. Jagust,William J. Jagust +17 more
TL;DR: In this paper, the authors defined patterns of tau tracer retention in normal aging in relation to age, cognition, and β-amyloid deposition, and found that older age was associated with increased tracers retention in regions of the medial temporal lobe, which predicted worse episodic memory performance.
Journal ArticleDOI
Tau PET patterns mirror clinical and neuroanatomical variability in Alzheimer's disease.
Rik Ossenkoppele,Rik Ossenkoppele,Rik Ossenkoppele,Daniel R. Schonhaut,Daniel R. Schonhaut,Michael Schöll,Michael Schöll,Samuel N. Lockhart,Nagehan Ayakta,Nagehan Ayakta,Suzanne L. Baker,James P. O'Neil,Mustafa Janabi,Andreas Lazaris,Averill Cantwell,Jacob W. Vogel,Miguel Santos,Zachary A. Miller,Brianne M. Bettcher,Brianne M. Bettcher,Keith A. Vossel,Joel H. Kramer,Maria Luisa Gorno-Tempini,Bruce L. Miller,William J. Jagust,William J. Jagust,Gil D. Rabinovici,Gil D. Rabinovici +27 more
TL;DR: Results are consistent with and expand upon findings from post-mortem, animal and cerebrospinal fluid studies, and suggest that the pathological aggregation of tau is closely linked to patterns of neurodegeneration and clinical manifestations of Alzheimer's disease.
Journal ArticleDOI
Tau pathology and neurodegeneration contribute to cognitive impairment in Alzheimer's disease.
Alexandre Bejanin,Daniel R. Schonhaut,Renaud La Joie,Joel H. Kramer,Suzanne L. Baker,Natasha Sosa,Nagehan Ayakta,Averill Cantwell,Mustafa Janabi,Mariella Lauriola,James P. O'Neil,Maria Luisa Gorno-Tempini,Zachary A. Miller,Howard J. Rosen,Bruce L. Miller,William J. Jagust,William J. Jagust,Gil D. Rabinovici,Gil D. Rabinovici,Gil D. Rabinovici +19 more
TL;DR: Results show that tau pathology is related in a region-specific manner to cognitive impairment in Alzheimer's disease, and regional relationships are weakly related to amyloid burden, but are in part mediated by grey matter volumes.
Journal ArticleDOI
Prospective longitudinal atrophy in Alzheimer’s disease correlates with the intensity and topography of baseline tau-PET
Renaud La Joie,Adrienne Visani,Suzanne L. Baker,Jesse A. Brown,Viktoriya Bourakova,Jungho Cha,Kiran Chaudhary,Lauren Edwards,Leonardo Iaccarino,Mustafa Janabi,Orit H. Lesman-Segev,Zachary A. Miller,David C. Perry,James P. O'Neil,Julie Pham,Julio C. Rojas,Howard J. Rosen,William W. Seeley,Richard M. Tsai,Bruce L. Miller,William J. Jagust,William J. Jagust,Gil D. Rabinovici +22 more
TL;DR: Quantitative analyses showed that the global intensity of tau-PET, but not β-amyloid–PET, signal predicted the rate of subsequent atrophy, independent of baseline cortical thickness, which support disease models in which tau pathology is a major driver of local neurodegeneration.
Journal ArticleDOI
Relationships between Beta-Amyloid and Functional Connectivity in Different Components of the Default Mode Network in Aging
Elizabeth C. Mormino,Andre Smiljic,Amynta O. Hayenga,Susan H. Onami,Michael D. Greicius,Gil D. Rabinovici,Mustafa Janabi,Suzanne L. Baker,Irene V. Yen,Cindee Madison,Bruce L. Miller,William J. Jagust +11 more
TL;DR: It is shown that DMN functional connectivity during rest is altered with increasing levels of PIB uptake in NC, and this pattern of decreases is consistent with previous studies that suggest heightened vulnerability of EM-related brain regions in AD, whereas the observed increases in FC may reflect a compensatory response.