Role of the blood-cerebrospinal fluid barrier to neuroinflammation and Alzheimer's disease

ZAMANI, Alemeh, Klaudia HAŠANOVÁ, Nir YAVIN, Václav BRÁZDA a Marek JOUKAL. Role of the blood-cerebrospinal fluid barrier to neuroinflammation and Alzheimer's disease. 2022.

Základní údaje

• Originální název: Role of the blood-cerebrospinal fluid barrier to neuroinflammation and Alzheimer's disease
• Autoři: ZAMANI, Alemeh, Klaudia HAŠANOVÁ, Nir YAVIN, Václav BRÁZDA a Marek JOUKAL.
• Vydání: 2022.

Další údaje

• Typ výsledku: Konferenční abstrakt
• Utajení: není předmětem státního či obchodního tajemství

Anotace

Alzheimer’s disease (AD) is a progressive neurodegenerative disorder where dementia gradually worsens over a number of years and becomes completely debilitating at later stages. Pathogenesis consists of amyloid-β peptide (Aβ) accumulation and tau protein clusters, leading to neuronal death. Choroid plexus (CP), forming the blood-cerebrospinal fluid barrier, plays a vital role in the clearance of the Aβ from the brain. During AD, insufficient clearance of Aβ and enhanced inflammatory changes in the CP and cerebrospinal fluid are observed. Despite its clinical importance, our knowledge of the role of the CP in the onset and progression of AD remains rather limited. This study deals with the role of the CP during AD and its potential relationship with neuroinflammation. Using immunocytochemistry, we investigated whether rat choroidal epithelial Z310 cell could uptake the Aβ and we observed Z310 cells responses to Aβ aggregation inside the cells. Aβ aggregation occurred in Z310 cells in a concentration- and time-dependent manner. According to this result, an in vitro model of AD was developed in which the expression of inflammatory mediators, and junctional proteins were examined. Initially, IL-1β expression increased, while tight junctions were downregulated. Interestingly, zonula occludens-1 returned to its normal level, and the occludin continued to decrease. IL-10 level after 5 days was upregulated. Our data show that Aβ aggregation causes an inflammatory response in the CP, which could potentially alter the structure of tight-junction proteins, which are essential for the functionality of the blood-cerebrospinal fluid barrier. In addition, the results support the protective nature of the CP during pathological conditions.