Author

Roberta Parolisi

Neuroscience Institute Cavalieri OttolenghiORCID 0000-0002-1948-7766Unclaimed ORCID profile · follow to get notified of new preprints

Biology Disciplines

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Neuroscience· 2 Genetics· 1

Signature Assays, Organisms & Methods

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Approach:experimental assay· 3 Organism:mouse· 2 Assay:bulk RNA-seq· 1 Research Focus:cell type annotation· 1 Research Focus:cell-cell communication· 1 Research Focus:differential expression· 1 Organism:human· 1

Frequent Co-Authors

Alfredo BruscoiD· 2 shared Annalisa BuffoiD· 2 shared Elisa GiorgioiD· 2 shared Francesca MontaroloiD· 2 shared Alessandro BrussinoiD· 1 shared Anna Maria PorcelliiD· 1 shared Antonio BertolottoiD· 1 shared Arianna Contato· 1 shared

Activity by Year

2018-2026 · peak 1/yr

Co-Author Collaboration Network

10 top collaborators · 29 mutual co-author links

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2 shared papersNeuroscience

Alfredo BruscoORCID

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3 papers

Recent·Most cited

NeurosciencebioRxivPreprintSep 15, 2026

Functional validation of allele-specific LMNB1 silencing in patient-derived astrocytes as a therapeutic option for Autosomal Dominant Leukodystrophy

Martina Lorenzati, Arianna Contato, Fernando Josa‐Prado…·Annalisa Buffo

This study validates allele-specific LMNB1 silencing in patient-derived astrocytes as a therapeutic approach for ADLD by showing restored physiological levels and functional improvements.

DOI 10.64898/2026.09.09.747273

humanbulk RNA-seq

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NeuroscienceEuropean Journal of NeurosciencePeer-reviewedNov 1, 2025

Acute particulate matter (PM10) exposure selectively triggers behavioral alterations in the presymptomatic Experimental Autoimmune Encephalomyelitis (EAE) mouse model of Multiple Sclerosis

Martino Bonato, Francesca Montarolo, Roberta Parolisi…·Enrica Boda

The paper shows that PM10 exposure affects behavior in presymptomatic EAE mice but not healthy mice, indicating a selective vulnerability in immunologically primed individuals.

DOI 10.1111/ejn.70304

mouseexperimental assay

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GeneticsNeurobiology of DiseasePeer-reviewedOct 30, 2018

Mice harboring a SCA28 patient mutation in AFG3L2 develop late-onset ataxia associated with enhanced mitochondrial proteotoxicity.

Cecilia Mancini, Eriola Hoxha, Luisa Iommarini…·Filippo Tempia

This study creates a new mouse model with a patient-derived SCA28 mutation and shows it leads to late-onset ataxia and mitochondrial dysfunction.

32 citations

mouseexperimental assay

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