Parkinson hastalığında AMPK'nin nörovasküler birim hasarındaki rolü ve mekanizmaları.

Araştırma özeti

Aşağıdaki metin kaynak makalenin lisansı doğrulanmış orijinal özetidir. cc by

Parkinson's disease (PD) is the second most common neurodegenerative disorder, characterized by dopaminergic neuron loss and α-synuclein aggregation. Increasing evidence indicates that blood-brain barrier (BBB) dysfunction in the neurovascular unit (NVU) is an early pathological event driving PD progression, rather than a secondary consequence. AMP-activated protein kinase (AMPK), a key cellular metabolic sensor, is activated by oxidative stress and endoplasmic reticulum stress induced by α-synuclein aggregates, and participates in regulating endothelial barrier function. This review systematically summarizes the pathological evidence of early BBB injury in PD, elaborates on the dual role of AMPK in BBB regulation, and highlights the value of phosphoproteomics in deciphering AMPK's downstream signaling networks. We propose the "α-synuclein-AMPK-phosphorylation network-BBB dysfunction" axis, discuss pharmacological clues from traditional Chinese medicine, and outline future research directions. This review provides a novel integrated perspective for understanding PD neurovascular pathology and lays a theoretical foundation for identifying early intervention targets by targeting AMPK-regulated NVU protection.

İlgili konular