Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems
Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. The classical hallmarks of AD include extracellular beta-amyloid (Aβ) plaques and neurofibrillary tau tangles, although they are often accompanied by various vascular defects. These changes...
| Main Authors: | , , |
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| Format: | Article |
| Language: | English |
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MDPI AG
2023-04-01
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| Series: | International Journal of Molecular Sciences |
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| Online Access: | https://www.mdpi.com/1422-0067/24/8/7046 |
| _version_ | 1797605125117706240 |
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| author | Ana Badimon Daniel Torrente Erin H. Norris |
| author_facet | Ana Badimon Daniel Torrente Erin H. Norris |
| author_sort | Ana Badimon |
| collection | DOAJ |
| description | Alzheimer’s disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. The classical hallmarks of AD include extracellular beta-amyloid (Aβ) plaques and neurofibrillary tau tangles, although they are often accompanied by various vascular defects. These changes include damage to the vasculature, a decrease in cerebral blood flow, and accumulation of Aβ along vessels, among others. Vascular dysfunction begins early in disease pathogenesis and may contribute to disease progression and cognitive dysfunction. In addition, patients with AD exhibit alterations in the plasma contact system and the fibrinolytic system, two pathways in the blood that regulate clotting and inflammation. Here, we explain the clinical manifestations of vascular deficits in AD. Further, we describe how changes in plasma contact activation and the fibrinolytic system may contribute to vascular dysfunction, inflammation, coagulation, and cognitive impairment in AD. Given this evidence, we propose novel therapies that may, alone or in combination, ameliorate AD progression in patients. |
| first_indexed | 2024-03-11T04:56:43Z |
| format | Article |
| id | doaj.art-064e78f45a2346feb46a1c0ff042c33c |
| institution | Directory Open Access Journal |
| issn | 1661-6596 1422-0067 |
| language | English |
| last_indexed | 2024-03-11T04:56:43Z |
| publishDate | 2023-04-01 |
| publisher | MDPI AG |
| record_format | Article |
| series | International Journal of Molecular Sciences |
| spelling | doaj.art-064e78f45a2346feb46a1c0ff042c33c2023-11-17T19:34:25ZengMDPI AGInternational Journal of Molecular Sciences1661-65961422-00672023-04-01248704610.3390/ijms24087046Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic SystemsAna Badimon0Daniel Torrente1Erin H. Norris2Patricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USAPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USAPatricia and John Rosenwald Laboratory of Neurobiology and Genetics, The Rockefeller University, 1230 York Avenue, New York, NY 10065, USAAlzheimer’s disease (AD) is the most common neurodegenerative disease, affecting millions of people worldwide. The classical hallmarks of AD include extracellular beta-amyloid (Aβ) plaques and neurofibrillary tau tangles, although they are often accompanied by various vascular defects. These changes include damage to the vasculature, a decrease in cerebral blood flow, and accumulation of Aβ along vessels, among others. Vascular dysfunction begins early in disease pathogenesis and may contribute to disease progression and cognitive dysfunction. In addition, patients with AD exhibit alterations in the plasma contact system and the fibrinolytic system, two pathways in the blood that regulate clotting and inflammation. Here, we explain the clinical manifestations of vascular deficits in AD. Further, we describe how changes in plasma contact activation and the fibrinolytic system may contribute to vascular dysfunction, inflammation, coagulation, and cognitive impairment in AD. Given this evidence, we propose novel therapies that may, alone or in combination, ameliorate AD progression in patients.https://www.mdpi.com/1422-0067/24/8/7046Alzheimer’s diseasecontact systemvasculaturefibrinogenbeta-amyloid |
| spellingShingle | Ana Badimon Daniel Torrente Erin H. Norris Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems International Journal of Molecular Sciences Alzheimer’s disease contact system vasculature fibrinogen beta-amyloid |
| title | Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems |
| title_full | Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems |
| title_fullStr | Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems |
| title_full_unstemmed | Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems |
| title_short | Vascular Dysfunction in Alzheimer’s Disease: Alterations in the Plasma Contact and Fibrinolytic Systems |
| title_sort | vascular dysfunction in alzheimer s disease alterations in the plasma contact and fibrinolytic systems |
| topic | Alzheimer’s disease contact system vasculature fibrinogen beta-amyloid |
| url | https://www.mdpi.com/1422-0067/24/8/7046 |
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