SCIENTIFIC HUB

Follow the evidence.

SCIENTIFIC LITERATURE · MED

The role and mechanisms of AMPK in neurovascular unit injury in Parkinson's disease.

Front Aging Neurosci · 2026-05-18

DOI: 10.3389/fnagi.2026.1790159PMID: 42232223

Open accessSystematic Review; systematic-review; Journal ArticleOriginal source ↗

Research overview

The text below is the source article’s original abstract under a verified reuse license. 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.

Scientific assessment

01

Research question

Assess the question within the original study’s scope.

02

Methods & sample

Check the source article for study design and sample details.

03

Key findings

An editorially approved findings summary is not yet published for this record.

04

Limitations

Generalizability, bias and clinical meaning require separate assessment.

Methods, samples and clinical conclusions are not inferred from bibliographic metadata.