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Basic Science and Pathogenesis.

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Alzheimer's disease and tau pathology shift brain endothelial cells to glycolysis, increasing inflammation and blood-brain barrier permeability. Restoring normal metabolism reverses these harmful effects, offering new therapeutic targets.

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Area of Science:

  • Neuroscience
  • Cell Biology
  • Biochemistry

Background:

  • Cerebral endothelial cells (cECs) are crucial for blood-brain barrier (BBB) integrity and neurovascular unit function.
  • Dysfunction of cECs contributes to neuroinflammation, neurodegeneration, and micro-hemorrhages observed in Alzheimer's disease (AD) and cerebral amyloid angiopathy (CAA).
  • Pathological amyloid-beta (Aβ) and tau aggregates alter cEC metabolism, promoting glycolysis and impairing mitochondrial function, which is linked to BBB permeability.

Purpose of the Study:

  • To investigate the mechanisms by which AD and CAA pathology alter cEC function.
  • To understand how cEC dysfunction mediates BBB and neurovascular alterations.
  • To explore the link between metabolic shifts in cECs and endothelial inflammatory activation and BBB permeability.

Main Methods:

  • Assessed mitochondrial respiration and glycolysis in human cECs using Seahorse Extracellular Flux Analyzer.
  • Measured BBB function via trans-endothelial electrical resistance (TEER) using the ECIS Zθ system.
  • Quantified endothelial inflammatory activation and vascular dysfunction pathways using MSD V-Plex Neuroinflammatory Panel, Western Blot, and immunofluorescence.
  • Investigated the effects of glycolysis inhibition on BBB and neurovascular dysfunction in vitro and in animal models of cerebral amyloidosis and tauopathy.

Main Results:

  • Both Aβ and tau aggregates induce a metabolic shift towards glycolysis in cECs, leading to inflammatory activation and BBB permeability.
  • Reducing glycolysis to normal levels can reverse the detrimental cerebrovascular effects caused by AD pathological aggregates.
  • Aβ directly switches cECs from mitochondrial respiration to glycolysis, while tau initially hyperactivates glycolysis, causing inflammation and BBB permeability, followed by mitochondrial dysfunction and cell death.
  • Key findings were confirmed in animal models of cerebral amyloidosis and tauopathy.

Conclusions:

  • A novel metabolic mechanism involving endothelial inflammatory activation and BBB pathology mediated by Aβ and tau species has been identified.
  • Targeting this metabolic pathway presents potential therapeutic strategies for AD, CAA, and tauopathies.
  • Interventions aimed at normalizing endothelial metabolism could limit immune cell infiltration and BBB permeability in neurodegenerative diseases.