Author

A. Demuro

Listed by name: these papers carry no ORCID for this author, so different people with the same name may be mixed together.

Biology Disciplines

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Cell Biology· 3

Signature Assays, Organisms & Methods

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Assay:electrophysiology· 3 Research Focus:cell signaling & trafficking· 2 Approach:experimental assay· 2 Organism:human· 2 Approach:deep learning· 1 Research Focus:host-pathogen & immune response· 1 Research Focus:protein folding & dynamics· 1 Approach:statistical model· 1

Frequent Co-Authors

G. Ullah· 3 shared I. Parker· 2 shared S. I. Shah· 2 shared A. Pensalfini· 1 shared A. R. Umar· 1 shared C. G. Glabe· 1 shared

Activity by Year

2022-2022 · peak 3/yr

Co-Author Collaboration Network

6 top collaborators · 12 mutual co-author links

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3 shared papersCell Biology

G. Ullah

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3 papers

Recent·Most cited

Modeling the kinetics of amyloid beta pores and long-term evolution of their Ca2+ toxicity

S. I. Shah, A. Demuro, G. Ullah

This study models the kinetics of amyloid beta pores and their long-term Ca2+ toxicity evolution, showing increasing toxicity due to pore number and activity over time.

bioRxiv · May 2, 2022 · PreprintCell Biology

Intracellular injection of brain extracts from Alzheimer's disease patients trigger unregulated Ca2+ release from intracellular stores that hinders cellular bioenergetics

A. Pensalfini, A. R. Umar, C. G. Glabe, I. Parker, G. Ullah, A. Demuro

The paper shows that brain extracts from Alzheimer's patients trigger unregulated Ca2+ release from intracellular stores, disrupting bioenergetics and supporting a role for amyloid oligomers in neuronal toxicity.

bioRxiv · Apr 29, 2022Cell Biology

Aβ42 and Aβ40 oligomers form transient and persistent pores with different time evolutions and toxicities

S. I. Shah, I. Parker, G. Ullah, A. Demuro

This study shows Aβ42 and Aβ40 oligomers form different Ca2+ permeable pores with distinct time-dependent toxicities in Alzheimer's disease.

bioRxiv · Apr 29, 2022 · PreprintCell Biology