ArticleBrain pathology (Zurich, Switzerland)2026
Dysregulated TIE-2 expression is associated with blood-brain barrier leakiness and Alzheimer's disease-related neuropathology.
Article in Brain pathology (Zurich, Switzerland), 2026. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 1 paper.
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1 citing paper in PubMed.
- Dysregulated TIE-2 expression in Alzheimer's disease: Further considerations on regional specificity and shedding evidence.Brain pathology (Zurich, Switzerland) · 2026Article
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13 authors.
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Abstract
Cerebral hypoperfusion and blood-brain barrier (BBB) leakiness are related to cognitive decline and the onset and spread of Aβ and tau pathology in Alzheimer's disease (AD). Disrupted angiopoietin/TIE (ANGPT/TIE) signalling causes neurovascular instability and BBB leakiness accelerating cognitive decline and disease pathology in mouse models of AD. To explore ANGPT/TIE signalling in human AD, we measured CSF TIE-1 and TIE-2 levels by ELISA in two independent clinical dementia cohorts, and serum and CSF Tie-1/-2 in paired CSF and serum samples from neurologically normal individuals. ANGPT1, ANGPT2, TIE-1 and TIE-2 levels were measured by ELISA in crude homogenate (CH) and microvessel-enriched fractions (MVFs) of post-mortem human parietal cortex in relation to biochemical markers of cerebral perfusion (MAG:PLP1) and BBB leakiness (parenchymal fibrinogen) in a control, AD, and vascular dementia (VaD) cohort. CSF soluble TIE-2 was elevated in AD biomarker+ve individuals and correlated positively with CSF t-tau and p-tau, and markers of BBB leakiness, neuronal injury, and neuroinflammation. Tissue TIE-2 levels were significantly reduced in Braak tangle stage (BS) III-IV, that is, brains with early-intermediate AD pathology, and were lower in MVFs in end-stage AD pathology (BSV-VI) than in controls or VaD. Lower levels of MVF TIE-2 correlated with markers of cerebral hypoperfusion and BBB leakiness. Our study reveals a reciprocal relationship between elevated CSF and reduced tissue TIE-2 expression that is related to markers of tau pathology, BBB leakiness, and cerebral hypoperfusion, providing novel insights into ANGPT/TIE signalling in AD.
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