ReviewFrontiers in neurology2025
Neurovascular coupling dysfunction in encephalopathy: pathophysiological advances and clinical implications.
Review in Frontiers in neurology, 2025. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers.
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Who cites it
6 citing papers in PubMed.
- PCSK9 in bridging metabolism and neurodegeneration: a new paradigm for alzheimer's treatment.Metabolic brain disease · 2026Review
- Eicosapentaenoic acid reprograms cerebrovascular metabolism and impairs repair after brain injury, with relevance to chronic traumatic encephalopathy.Cell reports · 2026Article
- Neurovascular Coupling Disruption and Glymphatic Dysfunction Are Associated With Visual Impairment in Pediatric Monocular Anisometropic Amblyopia.Investigative ophthalmology & visual science · 2026Article
- Targeting the astrocytic metabolic cascade in Alzheimer's disease: mechanisms, challenges and opportunities.Frontiers in aging neuroscience · 2026Review
- Noradrenergic Slow Vasomotion: The Hidden Fluid Pump Linking Sleep, Brain Clearance, and Dementia Pathogenesis.International journal of molecular sciences · 2025Review
- State-dependent facial pulsation asymmetry and phase asynchrony measured by imaging photoplethysmography and their coupling with contingent negative variation in migraine.Frontiers in neurologyArticle
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Authors and funding
5 authors.
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Abstract
Neurovascular coupling (NVC) is a sophisticated and vital physiological mechanism that ensures the brain's intricate balance and optimal performance. It refers to the precise coordination between the brain's neural activity and the local cerebral blood flow (CBF), which is essential for meeting the metabolic demands of active neurons. This coupling allows for the efficient delivery of oxygen and nutrients to brain regions experiencing increased activity and facilitates the removal of metabolic waste products. In encephalopathy, a collective term for a wide range of conditions that impair brain function, NVC dysfunction has been identified as a key factor contributing to the progression of these disorders and the emergence of clinical symptoms. This comprehensive review aims to explore the complex pathophysiological mechanisms that lead to NVC dysfunction in several encephalopathic conditions. These include but are not limited to Alzheimer's disease (AD), Parkinson's disease (PD), cerebral small vessel disease (CSVD), stroke, migraine, traumatic brain injury (TBI) and epilepsy. Across the spectrum of encephalopathies discussed in this review, a unifying molecular target emerges: endothelin-1 (ET-1) and its receptors. ET-1, a potent vasoconstrictor produced by endothelial cells and astrocytes, is intricately linked to NVC dysfunction in these conditions. A thorough understanding of the role of NVC in encephalopathic disorders can inform the development of diagnostic tools and therapeutic strategies. For instance, identifying early markers of NVC dysfunction could facilitate early intervention and potentially slow disease progression. Moreover, targeting the restoration of NVC could become a novel therapeutic approach to mitigate symptoms and improve patient outcomes. This review also proposes new directions for future research, encouraging the exploration of NVC's complex interactions and its potential as a therapeutic target in the management of encephalopathic conditions.
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