Blood-brain barrier alterations and their impact on Parkinson’s disease pathogenesis and therapy  

作　　者：Kristina Lau Rebecca Kotzur Franziska Richter 

机构地区：[1]Department of Pharmacology,Toxicology and Pharmacy,University of Veterinary Medicine Hannover,Foundation,Bünteweg 17,30559 Hannover,Germany [2]Center for Systems Neuroscience,Hannover,Germany

出　　处：《Translational Neurodegeneration》2024年第1期551-574,共24页转化神经变性病(英文)

基　　金：funded by intramural funds with no role in writing of the manuscript.

摘　　要：There is increasing evidence for blood-brain barrier(BBB)alterations in Parkinson’s disease(PD),the second most common neurodegenerative disorder with rapidly rising prevalence.Altered tight junction and transporter protein levels,accumulation ofα-synuclein and increase in inflammatory processes lead to extravasation of blood molecules and vessel degeneration.This could result in a self-perpetuating pathophysiology of inflammation and BBB alteration,which contribute to neurodegeneration.Toxin exposure orα-synuclein over-expression in animal models has been shown to initiate similar pathologies,providing a platform to study underlying mechanisms and therapeutic interventions.Here we provide a comprehensive review of the current knowledge on BBB alterations in PD patients and how rodent models that replicate some of these changes can be used to study disease mechanisms.Specific challenges in assessing the BBB in patients and in healthy controls are discussed.Finally,a potential role of BBB alterations in disease pathogenesis and possible implications for therapy are explored.The interference of BBB alterations with current and novel therapeutic strategies requires more attention.Brain region-specific BBB alterations could also open up novel opportunities to target specifically vulnerable neuronal subpopulations.

关 键 词：Neurovascular unit SYNUCLEINOPATHIES Α-SYNUCLEIN 

分 类 号：R742.5[医药卫生—神经病学与精神病学]