Publication details

Pathogenesis of Alzheimer´s disease: Involvement of the choroid plexus

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Authors

ČARNA Maria ONYANGO Isaac G. KATINA Stanislav HOLUB Dušan NOVOTNY Jan Sebastian NEZVEDOVÁ Markéta JHA Durga NEDELSKA Zuzana LACOVICH Valentina VYVERE Thijs Vande HOUBRECHTS Ruben GARCIA-MANSFIELD Krystine SHARMA Ritin DAVID-DIRGO Victoria VYHNALEK Martin TEXLOVA Kateřina CHAVES Hernan BAKKAR Nadine PERTIERRA Lucia VINKLER Mojmír MARKOVA Hana LACZO Jan SHEARDOVÁ Kateřina HORTOVA-KOHOUTKOVA Marcela FRIČ Jan FORTE Giancarlo KAŇOVSKY Petr BELAŠKOVA Silvie DAMBORSKÝ Jiří HORT Jakub SEYFRIED Nicholas T. BOWSER Robert SEVLEVER Gustavo RISSMAN Robert A. SMITH Richard A. HAJDUCH Marian PIRROTTE Patrick SPÁČIL Zdeněk DAMMER Eric B. LIMBÄCK-STOKIN Clara STOKIN Gorazd B.

Year of publication 2023
Type Article in Periodical
Magazine / Source Alzheimer´s & Dementia
MU Faculty or unit

Faculty of Science

Citation
Web DOI
Doi http://dx.doi.org/10.1002/alz.12970
Keywords aging; Alzheimer's disease; cerebrospinal fluid; choroid plexus; pathology
Attached files
Description The choroid plexus (ChP) produces and is bathed in the cerebrospinal fluid (CSF), which in aging and Alzheimer's disease (AD) shows extensive proteomic alterations including evidence of inflammation. Considering inflammation hampers functions of the involved tissues, the CSF abnormalities reported in these conditions are suggestive of ChP injury. Indeed, several studies document ChP damage in aging and AD, which nevertheless remains to be systematically characterized. We here report that the changes elicited in the CSF by AD are consistent with a perturbed aging process and accompanied by aberrant accumulation of inflammatory signals and metabolically active proteins in the ChP. Magnetic resonance imaging (MRI) imaging shows that these molecular aberrancies correspond to significant remodeling of ChP in AD, which correlates with aging and cognitive decline. Collectively, our preliminary post-mortem and in vivo findings reveal a repertoire of ChP pathologies indicative of its dysfunction and involvement in the pathogenesis of AD.
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