Blood-derived plasminogen drives brain inflammation and plaque deposition in a mouse model of Alzheimer’s disease

A Tale of Two Genes: Microglial Apoe and Trem2

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The TREM2-APOE Pathway Drives the Transcriptional Phenotype of Dysfunctional Microglia in Neurodegenerative Diseases

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Blood-Brain Barrier Dysfunction and the Pathogenesis of Alzheimer’s Disease

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Plasminogen Deficiency Delays the Onset and Protects from Demyelination and Paralysis in Autoimmune Neuroinflammatory Disease

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The plasminogen activation system in neuroinflammation

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Plasmin is a natural trigger for bradykinin production in patients with hereditary angioedema with factor XII mutations

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Role of thrombin in the pathogenesis of central nervous system inflammatory diseases

(2016) Safieh Ebrahimi et al.   JOURNAL OF CELLULAR PHYSIOLOGY

New tools for studying microglia in the mouse and human CNS

(2016) Mariko L. Bennett et al.   PROCEEDINGS OF THE NATIONAL ACADEMY OF SCIENCES OF THE UNITED STATES OF AMERICA

Fibrinolysis and the control of blood coagulation

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Impacts of aging and amyloid-β deposition on plasminogen activators and plasminogen activator inhibitor-1 in the Tg2576 mouse model of Alzheimer׳s disease

(2015) Shin Bi Oh et al.   BRAIN RESEARCH

Neuroinflammation in Alzheimer's disease

(2015) Michael T Heneka et al.   LANCET NEUROLOGY

Innate immunity in Alzheimer's disease

(2015) Michael T Heneka et al.   NATURE IMMUNOLOGY

TMEM119 marks a subset of microglia in the human brain

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Activation of the factor XII-driven contact system in Alzheimer’s disease patient and mouse model plasma

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Breaking boundaries—coagulation and fibrinolysis at the neurovascular interface

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Plasminogen promotes macrophage phagocytosis in mice

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Plasmin deficiency leads to fibrin accumulation and a compromised inflammatory response in the mouse brain

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Temporal gene profiling of the 5XFAD transgenic mouse model highlights the importance of microglial activation in Alzheimer’s disease

(2014) Véréna Landel et al.   Molecular Neurodegeneration

Microglia, neuroinflammation, and beta-amyloid protein in Alzheimer's disease

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Cytokines and Chemokines at the Crossroads of Neuroinflammation, Neurodegeneration, and Neuropathic Pain

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Microglia and macrophages of the central nervous system: the contribution of microglia priming and systemic inflammation to chronic neurodegeneration

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Microglia and Inflammation in Alzheimers Disease

(2012) Shweta Mandrekar-Colucci et al.   CNS & Neurological Disorders-Drug Targets

The immunology of neurodegeneration

(2012) Eva Czirr et al.   JOURNAL OF CLINICAL INVESTIGATION

Plasmin as a proinflammatory cell activator

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Regulation of macrophage migration by a novel plasminogen receptor Plg-RKT

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Inflammation and Alzheimer’s disease

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Mechanisms Underlying Inflammation in Neurodegeneration

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Genetically Modified CD34+ Hematopoietic Stem Cells Contribute to Turnover of Brain Perivascular Macrophages in Long-Term Repopulated Primates

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The effect of non-steroidal anti-inflammatory agents on behavioural changes and cytokine production following systemic inflammation: Implications for a role of COX-1

(2009) J.L. Teeling et al.   BRAIN BEHAVIOR AND IMMUNITY

Cholinergic control of inflammation

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Knockout of plasminogen activator inhibitor 1 gene reduces amyloid beta peptide burden in a mouse model of Alzheimer's disease

(2009) R.-M. Liu et al.   NEUROBIOLOGY OF AGING

The Neurology of the Immune System: Neural Reflexes Regulate Immunity

(2009) Mauricio Rosas-Ballina et al.   NEURON

Inflammation in Alzheimer's disease: Amyloid-β oligomers trigger innate immunity defence via pattern recognition receptors

(2009) Antero Salminen et al.   PROGRESS IN NEUROBIOLOGY

A leaky blood-brain barrier, fibrinogen infiltration and microglial reactivity in inflamed Alzheimer’s disease brain

(2008) Jae K. Ryu et al.   JOURNAL OF CELLULAR AND MOLECULAR MEDICINE

Inflammatory macrophage migration requires MMP-9 activation by plasminogen in mice

(2008) Yanqing Gong et al.   JOURNAL OF CLINICAL INVESTIGATION

Neuro-inflammation induced by lipopolysaccharide causes cognitive impairment through enhancement of beta-amyloid generation

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