CEREBROSPINAL FLUID AND PLASMA RHEOLOGY IN ALZHEIMER’S DISEASE - INDUCED RATS

Alzheimer’s disease (AD) is a neurodegenerative disorder characterized by progressive cognitive decline and neuropathological changes. Emerging evidence suggests that AD may also influence cerebrospinal fluid (CSF) composition and plasma rheology, which could play a role in disease progression. This study aimed investigatigating possible alterations in CSF cellular composition and plasma rheological properties such as plasma fibrinogen concentration and plasma viscosity in a rat model of AD. Twelve (12) healthy adult wistar rats weighing between 170-190g were used for this study. The rats were divided into two groups: Group 1 as control (n=6) received water, Group 2 (n=6) were induced with Alzheimer’s disease. Aluminum chloride salt (Alcl3) was used to induce Alzheimer’s disease, 100mg of Alcl3 salt was dissolved in 10ml of distilled water to achieve a concentration of 100mg/ml. 1ml of this solution was administered intraperitoneally daily for 28 days. Weight of rats were taken weekly, at the end of the experimental period, the rats were sacrificed, blood and CSF samples were collected. Cerebrospinal fluid analysis was performed using microscopy cell counting method, plasma fibrinogen concentration was determined by the clot-weight technique of Ingram and plasma viscosity was determined using the simple viscometer technique. All statistical analysis were carried out using t-test with graph pad prism 10.2.2. Results were presented as standard error of mean (SEM). Analysis of variance (ANOVA) was used to compare the means of tests and control value and a p-value of less than 0.05 was considered statistically significant. Results showed that Alzheimer's disease did not cause significant changes in CSF cellular components. Plasma viscosity remained unchanged between the Alzheimer-induced group and the control. However, plasma fibrinogen concentration was significantly increased in the Alzheimer-induced group, Increased fibrinogen in this study may indicate early-stage neuroinflammation but not enough to alter plasma viscosity. This may lead to hypercoagulability increasing the risk of blood clots, potentially reducing cerebral blood flow and raising the likelihood of stroke and vascular dementia. Additionally, impaired circulation from elevated fibrinogen may decrease oxygen and glucose delivery to the brain, contributing to neuronal stress and cognitive decline. This highlights a crucial link between systemic inflammation and neurodegeneration. In conclusion, this finding suggests that in this Alzheimer’s model systemic inflammation was present due to elevated plasma fibrinogen but the lack of CSF cellular changes and stable plasma viscosity indicate minimal neuroinflammation and an intact blood-brain barrier.