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Thinking outside the black box:are the brain endothelial cells the new main target in Alzheimer's disease?

Neural Regeneration Research 2023年第12期18卷 2592-2598页

作者： Enrique Estudillo Adolfo López-Ornelas Alejandro Rodríguez-Oviedo Neptali Gutiérrez de la Cruz Marco Antonio Vargas-Hernández Adriana Jiménez Laboratorio de Reprogramación Celular Instituto Nacional de Neurología y Neurocirugía Manuel Velasco SuárezMexico CityMexico División de Investigación Hospital Juárez de MéxicoMexico CityMexico Hospital Nacional Homeopático Hospitales Federales de ReferenciaMexico CityMexico Facultad de Ciencias Universidad Nacional Autónoma de MéxicoMexico CityMexico Laboratorio de Morfología Escuela Militar de Graduados de SanidadSecretaría de la Defensa NacionalBatalla de CelayaLomas de SoteloMiguel HidalgoMexico CityMexico Escuela Militar de Graduados de Sanidad Secretaría de la Defensa NacionalBatalla de CelayaLomas de SoteloMiguel HidalgoMexico CityMexico

The blood-brain barrier is the interface through which the brain interacts with the milieu and consists mainly of a sophisticated network of brain endothelial cells that forms blood vessels and selectively moves molecules inside and outside the brain through multiple mechanisms of transport.Although brain endothelial cell function is crucial for brain homeostasis,their role in neurodegenerative diseases has historically not been considered with the same importance as other brain cells such as microglia,astroglia,neurons,or even molecules such as amyloid beta,Tau,or alpha-synuclein.Alzheimer's disease is the most common neurodegenerative disease,and brain endothelial cell dysfunction has been reported by several groups.However,its impairment has barely been considered as a potential therapeutic target.Here we review the most recent advances in the relationship between Alzheimer's disease and brain endothelial cells commitment and analyze the possible mechanisms through which their alterations contribute to this neurodegenerative disease,highlighting their inflammatory phenotype and the possibility of an impaired secretory pattern of brain endothelial cells that could contribute to the progression of this ailment.Finally,we discuss why shall brain endothelial cells be appreciated as a therapeutic target instead of solely an obstacle for delivering treatments to the injured brain in Alzheimer's disease.

关键词： dementia endothelial cells neurodegeneration neuroinflammation neuronal death paracellular transport transcellular transport

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Defective claudin-10 causes a novel variation of HELIX syndrome through compromised tight junction strand assembly

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Genes & Diseases 2022年第5期9卷 1301-1314页

作者： Sebastian Sewerin Jorg Piontek Ria Schonauer Sonja Grunewald Angelika Rauch Steffen Neuber Carsten Bergmann Dorothee Gunzel Jan Halbritte Division of Nephrology University of Leipzig Medical CenterLeipzig 04103Germany Clinical Physiology/Nutritional Medicine Charitee Universitatsmedizin BerlinBerlin 12203Germany Division of Dermatology Venereologyand AllergologyUniversity of Leipzig Medical CenterLeipzig 04103Germany Division of Prosthodontics and Materials Science University of Leipzig Medical CenterLeipzig 04103Germany Center for Human Genetics BioscientiaIngelheim 55218Germany f Medizinische Genetik MainzLimbach GeneticsMainz 55128Germany

Formation of claudin-10 based tight junctions(TJs)is paramount to paracellular Na+transport in multiple epithelia.Sequence variants in CLDN10 have been linked to HELIX syndrome,a salt-losing tubulopathy with altered handling of divalent cations accompanied by dysfunctional salivary,sweat,and lacrimal glands.Here,we investigate molecular basis and phenotypic consequences of a newly identified homozygous CLDN10 variant that translates into a single amino acid substitution within the fourth transmembrane helix of claudin-10.In addition to hypohidrosis(H),electrolyte(E)imbalance with impaired urine concentrating ability,and hypolacrimia(L),phenotypic findings include altered salivary electrolyte composition and amelogenesis imperfecta but neither ichthyosis(I)nor xerostomia(X).Employing cellular TJ reconstitution assays,we demonstrate perturbation of cis-and trans-interactions between mutant claudin-10 proteins.Ultrastructures of reconstituted TJ strands show disturbed continuity and reduced abundance in the mutant case.Throughout,both major isoforms,claudin-10a and claudin-10b,are differentially affected with claudin-10b showing more severe molecular alterations.However,expression of the mutant in renal epithelial cells with endogenous TJs results in wild-type-like ion selectivity and conductivity,indicating that aberrant claudin-10 is generally capable of forming functional paracellular channels.Thus,mutant proteins prove pathogenic by compromising claudin-10 TJ strand assembly.Additional ex vivo investigations indicate their insertion into TJs to occur in a tissue-specific manner.

关键词： Claudin-10 HELIX syndrome paracellular transport Salt-losing tubulopathy Tight junction

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