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Anne M. Cataldo
Researcher at Harvard University
Publications - 64
Citations - 9972
Anne M. Cataldo is an academic researcher from Harvard University. The author has contributed to research in topics: Endosome & Alzheimer's disease. The author has an hindex of 41, co-authored 64 publications receiving 9239 citations. Previous affiliations of Anne M. Cataldo include McLean Hospital & New York University.
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Extensive involvement of autophagy in Alzheimer disease: an immuno-electron microscopy study.
Ralph A. Nixon,Ralph A. Nixon,Jerzy Wegiel,Asok Kumar,Asok Kumar,Wai Haung Yu,Wai Haung Yu,Corrinne M. Peterhoff,Anne M. Cataldo,Anne M. Cataldo,Ana Maria Cuervo +10 more
TL;DR: This work unequivocally identified autophagosomes and other prelysosomal autophagic vacuoles (AVs), which were morphologically and biochemically similar to AVs highly purified from mouse liver, and provides the first evidence that macroautophagy is extensively involved in the neurodegenerative/regenerative process in AD.
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Macroautophagy—a novel β-amyloid peptide-generating pathway activated in Alzheimer's disease
W. Haung Yu,Ana Maria Cuervo,Asok Kumar,Corrinne M. Peterhoff,Stephen D. Schmidt,Ju-Hyun Lee,Ju-Hyun Lee,Panaiyur S. Mohan,Panaiyur S. Mohan,Marc Mercken,Mark R. Farmery,Lars O. Tjernberg,Ying Jiang,Ying Jiang,Karen Duff,Karen Duff,Yasuo Uchiyama,Jan Näslund,Paul M. Mathews,Paul M. Mathews,Anne M. Cataldo,Ralph A. Nixon,Ralph A. Nixon +22 more
TL;DR: It is shown that neuronal macroautophagy is induced early in Alzheimer's disease (AD) and before β-amyloid (Aβ) deposits extracellularly in the presenilin (PS) 1/Aβ precursor protein (APP) mouse model of β- amyloidosis.
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Endocytic Pathway Abnormalities Precede Amyloid β Deposition in Sporadic Alzheimer’s Disease and Down Syndrome : Differential Effects of APOE Genotype and Presenilin Mutations
Anne M. Cataldo,Corrinne M. Peterhoff,Juan C. Troncoso,Teresa Gomez-Isla,Bradley T. Hyman,Ralph A. Nixon +5 more
TL;DR: Early endosomal abnormalities provide a mechanistic link between EP alterations, genetic susceptibility factors, and Abeta generation and suggest differences that may be involved in Abetageneration and beta amyloidogenesis in subtypes of AD.
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Increased Neuronal Endocytosis and Protease Delivery to Early Endosomes in Sporadic Alzheimer’s Disease: Neuropathologic Evidence for a Mechanism of Increased β-Amyloidogenesis
TL;DR: Enhanced endocytic activity, coupled with increased trafficking to endosomes of proteases, constitutes a potential mechanism by which β-amyloidogenesis may become accelerated in sporadic AD and also be subject to influences by ApoE.
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Enzymatically active lysosomal proteases are associated with amyloid deposits in Alzheimer brain.
Anne M. Cataldo,Ralph A. Nixon +1 more
TL;DR: The high levels of enzymatically competent lysosomal proteases abnormally localized in senile plaques represent evidence for candidate enzymes that may mediate the proteolytic formation of amyloid.