Author

Felipe Campos Ribeiro

Universidade Federal do Rio de JaneiroORCID 0000-0003-3028-3307Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 3

Signature Assays, Organisms & Methods

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Research Focus:differential expression· 3 Organism:mouse· 3 Assay:proteomics· 3 Research Focus:cell-cell communication· 2 Research Focus:drug response / drug discovery· 2 Approach:experimental assay· 2 Approach:statistical model· 2 Research Focus:cell type annotation· 1

Frequent Co-Authors

Mychael V. LourencoiD· 3 shared Sergio Teixeira FerreiraiD· 3 shared Argel Aguilar‐VallesiD· 2 shared Danielle CozachencoiD· 2 shared Fernanda G. De FeliceiD· 2 shared Jean‐Claude LacailleiD· 2 shared Karim NaderiD· 2 shared Nahum SonenbergiD· 2 shared

Activity by Year

2021-2025 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 45 mutual co-author links

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3 shared papersNeuroscience

Mychael V. LourencoORCID

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3 papers

Recent·Most cited

NeuroscienceAging CellPeer-reviewedDec 3, 2025

Genetic reduction of the translational repressors FMRP and 4E-BP2 preserves memory in mouse models of Alzheimer's disease

Felipe Campos Ribeiro, Danielle Cozachenco, Michael Parkhill…·Sergio Teixeira Ferreira

This study shows that reducing FMRP and 4E-BP2 in mice prevents memory loss caused by Alzheimer's disease-linked amyloid-beta oligomers.

8 citationstop 4%

mouseproteomics

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NeuroscienceAlzheimer s & DementiaPeer-reviewedJun 27, 2024

The ketamine metabolite (2R,6R)-hydroxynorketamine rescues hippocampal mRNA translation, synaptic plasticity and memory in mouse models of Alzheimer's disease

Felipe Campos Ribeiro, Danielle Cozachenco, Elentina K. Argyrousi…·Sergio Teixeira Ferreira

19 citationstop 3%

mouseproteomics

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NeurosciencebioRxivPreprintNov 12, 2021

Age-linked suppression of lipoxin A4 mediates cognitive deficits in mice and humans

Fabrício A. Pamplona, Gabriela Vitória, Felipe Campos Ribeiro…·Fernanda Freire Tovar-Moll

This study shows that reduced lipoxin A4 levels in aging brains contribute to cognitive deficits in mice and humans, suggesting LXA4 as a potential therapeutic target for age-related dementia.

2 citations

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