Full Text Available
Note: Clicking the button above will open the full text document at the original institutional repository in a new window.
Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia
Thesis (PhD (Human Physiology))--University of Pretoria, 2015.
Saved in:
| Other Authors: | |
|---|---|
| Format: | Thesis |
| Language: | English |
| Published: |
2026
|
| Subjects: | |
| Tags: |
No Tags, Be the first to tag this record!
|
| _version_ | 1867613499502362624 |
|---|---|
| access_status_str | Open Access |
| author2 | Pretorius, E. |
| author_browse | Pretorius, E. |
| author_facet | Pretorius, E. |
| collection | Thesis |
| description | Thesis (PhD (Human Physiology))--University of Pretoria, 2015. |
| format | Thesis |
| id | oai:repository.up.ac.za:2263/110131 |
| institution | University of Pretoria (South Africa) |
| language | English |
| last_indexed | 2026-06-10T12:37:07.296Z |
| license_str | Not specified — see source repository |
| provenance_str_mv | Harvested via OAI-PMH from UPSpace — University of Pretoria Institutional Repository |
| publishDate | 2026 |
| publishDateRange | 2026 |
| publishDateSort | 2026 |
| record_format | dspace |
| source_str | UPSpace — University of Pretoria Institutional Repository |
| spelling | oai:repository.up.ac.za:2263/110131 Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia Pretorius, E. janette.bester@up.ac.za Bester, Janette Alzheimers disease Coagulation Ultrastructure Inflammation Thesis (PhD (Human Physiology))--University of Pretoria, 2015. Alzheimer-type dementia (AD) is a neurodegenerative disorder and the most common form of dementia. Patients typically present with neuro- and systemic inflammation and iron dysregulation, associated with oxidative damage that reflects in hypercoagulability. Hypercoagulability is closely associated with increased fibrinogen and in AD patients’ fibrinogen has been implicated in the development of neuroinflammation and memory deficits. There is still no clear reason precisely why (a) this hypercoagulable state, (b) iron dysregulation and (c) increased fibrinogen could together lead to the loss of neuronal structure and cognitive function. The current study suggests an alternative hypothesis based on previous ultrastructural evidence of the presence of a (dormant) blood microbiome in AD. Furthermore, this study will argue that bacterial cell wall components, such as the endotoxin lipopolysaccharide (LPS) of Gram-negative strains, might be the cause of the continuing and low-grade inflammation, characteristic of AD. An integrated approach was taken, by studying the viscoelastic and ultrastructural properties of AD and aged related control plasma as well as whole blood by using scanning electron microscopy, Thromboelastography (TEG®), the Global Thrombosis Test (GTT®), confocal microscopy and haematological parameters. No abnormalities were noticed when the general routine tests (complete blood count and iron profiles) were done between the AD and control group. Ultrastructural analysis however, confirmed the expected changes and ii deformed morphology of erythrocytes in AD patients due to damage of the membrane. TEG® analysis showed a hypercoagulable state in AD. TEG® results where LPS was added to naive blood showed the same trends as were found with the AD patients, while the GTT® results (where only platelet activity is measured), were not affected by the added LPS, suggesting that LPS does not directly impact platelet function. Confocal microscopy also confirmed the membrane damage via a biochemical techniques using fluorescent markers that mark the proteins responsible for RBC stability and integrity. Through this techniques an evident difference of the protein arrangement was noticed between the AD and the control group. These findings reinforce the importance of further investigating the role of LPS in AD. Physiology PhD (Human Physiology) 2026-05-15T17:26:23Z 2026-05-15T17:26:23Z 16/03/16 2015 Thesis http://hdl.handle.net/2263/110131 en application/pdf |
| spellingShingle | Alzheimers disease Coagulation Ultrastructure Inflammation Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title | Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title_full | Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title_fullStr | Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title_full_unstemmed | Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title_short | Lipopolysaccharide promotes hypercoagulability in Alzheimer’s type dementia |
| title_sort | lipopolysaccharide promotes hypercoagulability in alzheimer s type dementia |
| topic | Alzheimers disease Coagulation Ultrastructure Inflammation |
| url | http://hdl.handle.net/2263/110131 |