Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease: Identifying New Biomarkers Mirroring Metabolic Alterations

Pasquale Mone; Antonio De Luca; Urna Kansakar; Gaetano Santulli

doi:10.3233/JAD-231464

Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease: Identifying New Biomarkers Mirroring Metabolic Alterations

Pasquale Mone, Antonio De Luca, Urna Kansakar, Gaetano Santulli

Medicine

Research output: Contribution to journal › Review article › peer-review

Abstract

Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid-β accumulation, tau dysfunction, and neuroinflammation, involving endothelial cells and leukocytes. The breakdown of the blood-brain barrier allows immune cell infiltration, intensifying inflammation. A decreased ratio of Connexin-37 (Cx37, also known as GJA4: Gap Junction Protein Alpha 4) and Prolyl Hydroxylase Domain-Containing Protein 3 (PHD3, also known as EGLN3: Egl-9 Family Hypoxia Inducible Factor 3), Cx37/PHD3, consistently observed in different AD-related models, may represent a novel potential biomarker of AD, albeit the exact mechanisms underlying this phenomenon, most likely based on gap junction-mediated cellular interaction that modulate the cellular metabolite status, remain to be fully elucidated.

Original language	English (US)
Pages (from-to)	1685-1687
Number of pages	3
Journal	Journal of Alzheimer's Disease
Volume	97
Issue number	4
DOIs	https://doi.org/10.3233/JAD-231464
State	Published - Feb 13 2024

Keywords

Alzheimer's disease
Cx37
PHD3
blood-brain barrier
endothelial cells
inflammation

ASJC Scopus subject areas

General Neuroscience
Clinical Psychology
Geriatrics and Gerontology
Psychiatry and Mental health

UN SDGs

This output contributes to the following UN Sustainable Development Goals (SDGs)

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10.3233/JAD-231464

Cite this

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title = "Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease: Identifying New Biomarkers Mirroring Metabolic Alterations",

abstract = "Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid-β accumulation, tau dysfunction, and neuroinflammation, involving endothelial cells and leukocytes. The breakdown of the blood-brain barrier allows immune cell infiltration, intensifying inflammation. A decreased ratio of Connexin-37 (Cx37, also known as GJA4: Gap Junction Protein Alpha 4) and Prolyl Hydroxylase Domain-Containing Protein 3 (PHD3, also known as EGLN3: Egl-9 Family Hypoxia Inducible Factor 3), Cx37/PHD3, consistently observed in different AD-related models, may represent a novel potential biomarker of AD, albeit the exact mechanisms underlying this phenomenon, most likely based on gap junction-mediated cellular interaction that modulate the cellular metabolite status, remain to be fully elucidated.",

keywords = "Alzheimer's disease, Cx37, PHD3, blood-brain barrier, endothelial cells, inflammation",

author = "Pasquale Mone and {De Luca}, Antonio and Urna Kansakar and Gaetano Santulli",

year = "2024",

month = feb,

day = "13",

doi = "10.3233/JAD-231464",

language = "English (US)",

volume = "97",

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journal = "Journal of Alzheimer's Disease",

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T1 - Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease

T2 - Identifying New Biomarkers Mirroring Metabolic Alterations

AU - Mone, Pasquale

AU - De Luca, Antonio

AU - Kansakar, Urna

AU - Santulli, Gaetano

PY - 2024/2/13

Y1 - 2024/2/13

N2 - Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid-β accumulation, tau dysfunction, and neuroinflammation, involving endothelial cells and leukocytes. The breakdown of the blood-brain barrier allows immune cell infiltration, intensifying inflammation. A decreased ratio of Connexin-37 (Cx37, also known as GJA4: Gap Junction Protein Alpha 4) and Prolyl Hydroxylase Domain-Containing Protein 3 (PHD3, also known as EGLN3: Egl-9 Family Hypoxia Inducible Factor 3), Cx37/PHD3, consistently observed in different AD-related models, may represent a novel potential biomarker of AD, albeit the exact mechanisms underlying this phenomenon, most likely based on gap junction-mediated cellular interaction that modulate the cellular metabolite status, remain to be fully elucidated.

AB - Alzheimer's disease (AD) is a neurodegenerative disorder marked by amyloid-β accumulation, tau dysfunction, and neuroinflammation, involving endothelial cells and leukocytes. The breakdown of the blood-brain barrier allows immune cell infiltration, intensifying inflammation. A decreased ratio of Connexin-37 (Cx37, also known as GJA4: Gap Junction Protein Alpha 4) and Prolyl Hydroxylase Domain-Containing Protein 3 (PHD3, also known as EGLN3: Egl-9 Family Hypoxia Inducible Factor 3), Cx37/PHD3, consistently observed in different AD-related models, may represent a novel potential biomarker of AD, albeit the exact mechanisms underlying this phenomenon, most likely based on gap junction-mediated cellular interaction that modulate the cellular metabolite status, remain to be fully elucidated.

KW - Alzheimer's disease

KW - Cx37

KW - PHD3

KW - blood-brain barrier

KW - endothelial cells

KW - inflammation

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U2 - 10.3233/JAD-231464

DO - 10.3233/JAD-231464

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SN - 1387-2877

VL - 97

SP - 1685

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JO - Journal of Alzheimer's Disease

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ER -

Leukocytes and Endothelial Cells Participate in the Pathogenesis of Alzheimer's Disease: Identifying New Biomarkers Mirroring Metabolic Alterations

Abstract

Keywords

ASJC Scopus subject areas

UN SDGs

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