NEUROINFLAMMATION AND ITS IMPACT ON COGNITIVE DECLINE IN ALZHEIMER'S DISEASE.

Abstract

Background: Alzheimer’s disease, neuroinflammation has been found to play a part in further worsening of the events that lead to dementia. Inflammation from activated microglia and astrocytes increase the output of pro-inflammatory cytokines to amplify neuronal lesion. It seems that knowledge of neuroinflammation involvement in AD could give a clue about how, controlling the inflammation process, we can help stop or reverse the progressive cognitive worsening in AD.
Objectives: To study the link between neuroinflammation and cognitive dysfunction in Alzheimer’s disease and to analyze how data on certain inflammatory indicators can help determine the extent of cognitive dysfunction, as well as to consider possible further therapeutic strategies for inhibiting neuroinflammation in the course of the disease.
Study design: A cross-sectional, descriptive study.
Place and duration of study: Northwest General Hospital Peshawar from jan 2022 to March 2022
Methods: 100 AD patients and neuroinflammation (IL-1β, TNF-α, IL-6) and cognition scores were compared. Peripheral blood samples were tested for selected inflammatory cytokines and patients’ cognitive status was evaluated with the MMSE. To find the effect of neuroinflammation on cognition, statistical t-test, correlation, and regression analysis were conducted on data retrieved from the patients.
Results:100 Alzheimer’s patients with mean age of 72.5 years (±8.3 Standard Deviation). There was also a positive significant relationship between pro-inflammatory cytokines (IL 1- beta, TNF-alpha, IL-6) and low MMSE scores. There were statistically significant differences between the groups of patients, significant in higher cytokine levels (more severe dementia) showed higher declines in performance. Sustained cytokine levels were also shown to be highly significant by regression analysis, suggesting that cognitive deterioration did indeed correlate directly with cytokine levels. Taken together, these results implicating neuroinflammation in furthering cognitive impairment in Alzheimer disease are well supported.
Conclusion: According to the research presented, positive findings were obtained showing that neuroinflammation and, therefore, higher pro-inflammatory cytokines are a direct cause of cognitive impairments in Alzheimer’s disease. Inhibition of neuroinflammatory pathways could therefore represent an early and effective treatment strategy to forestall the progressive intolerance to cognitive dysfunctions of the disease and its pace of progression. It will thus be necessary for future work to establish new therapies that might allow suppressing inflammation to slow down the progression of Ad’s cognitive decline.