Main Article Content

Sarwat Ali Raja
Rabia Saleem
Waqas Ahmed
Dr Asnad



Introduction: Alzheimer's Disease (AD) is a devastating neurodegenerative disorder that poses a growing global health challenge as our population ages.

Objectives: The basic aim of the study is to find the biochemical pathways of alzheimer’s disease amyloid beta and tau protein dynamics.

Material and methods: This research study employed a cross-sectional design to investigate the biochemical pathways associated with Alzheimer's Disease, specifically focusing on amyloid beta (Aβ) and tau protein dynamics. A total of 80 participants were recruited for this study.  Participants underwent a comprehensive clinical assessment, including medical history, physical examination, and review of medical records. To assess cognitive function and disease severity, standardized neuropsychological tests were administered, including the Mini-Mental State Examination (MMSE), the Alzheimer's Disease Assessment Scale-Cognitive Subscale (ADAS-Cog), and other relevant cognitive assessments.

Results: Data was collected from 80 patients of AD. Mean age of the patients was 75.2 ± 6.1 years. There were 36 male and 44 female patients. Cerebrospinal fluid (CSF) analysis showed that the average Aβ42 concentration was 150 pg/mL (SD = 25) among participants. Tau protein levels in CSF averaged 550 pg/mL (SD = 100). Notably, there was a significant negative correlation between Aβ42 levels and MMSE scores (r = -0.45, p < 0.001), indicating that lower Aβ42 concentrations were associated with more severe cognitive impairment.

Conclusion: It is concluded that there is a significant association between Aβ and tau protein dynamics, biomarker levels, brain imaging findings, and cognitive impairment. These results contribute to our understanding of Alzheimer's Disease pathophysiology and have implications for future research and potential interventions in this devastating condition.

Abstract 87 | PDF Downloads 34


1. Guo, T., Zhang, D., Zeng, Y. et al. Molecular and cellular mechanisms underlying the pathogenesis of Alzheimer’s disease. Mol Neurodegeneration 15, 40 (2020).
2. Pogue AI, Lukiw WJ. Up-regulated pro-inflammatory MicroRNAs (miRNAs) in Alzheimer’s disease (AD) and age-related macular degeneration (AMD). Cell Mol Neurobiol. 2018;38 (5): 1021–31.
3. Arvanitakis Z, et al. Relation of cerebral vessel disease to Alzheimer’s disease dementia and cognitive function in elderly people: a cross-sectional study. Lancet Neurol. 2016;15(9):934–43.
4. Nelson AR, et al. Neurovascular dysfunction and neurodegeneration in dementia and Alzheimer’s disease. Biochim Biophys Acta. 2016;1862(5):887–900.
5. Sweeney MD, Sagare AP, Zlokovic BV. Blood-brain barrier breakdown in Alzheimer disease and other neurodegenerative disorders. Nat Rev Neurol. 2018;14(3):133–50.
6. Yiannopoulou KG, et al. Reasons for failed trials of disease-modifying treatments for alzheimer disease and their contribution in recent research. Biomedicines. 2019;7(4):97.
7. Iliyasu, Musa O., et al. "Amyloid-beta Aggregation Implicates Multiple Pathways in Alzheimer’S Disease: Understanding the Mechanisms." Frontiers in Neuro
science, vol. 17, 2023, p. 1081938,
8. Hampel, Harald, et al. "The Amyloid-β Pathway in Alzheimer’S Disease." Molecular Psychiatry, vol. 26, no. 10, 2021, pp. 5481-5503,
9. Calabrò M, Rinaldi C, Santoro G, Crisafulli C. The biological pathways of Alzheimer disease: a review. AIMS Neurosci. 2020 Dec 16;8(1):86-132. doi: 10.3934/Neuroscience.2021005. PMID: 33490374; PMCID: PMC7815481.
10. Holsinger RM, Goense N, Bohorquez J, et al. Splice variants of the Alzheimer's disease beta-secretase, BACE1. Neurogenetics. 2013;14:1–9
11. Gulisano W, Maugeri D, Baltrons MA, Fà M, Amato A, Palmeri A, D'Adamio L, Grassi C, Devanand DP, Honig LS, Puzzo D, Arancio O. Role of Amyloid-β and Tau Proteins in Alzheimer's Disease: Confuting the Amyloid Cascade. J Alzheimers Dis. 2018;64(s1):S611-S631. doi: 10.3233/JAD-179935. Erratum in: J Alzheimers Dis. 2019;68(1):415. PMID: 29865055; PMCID: PMC8371153.
12. Penke, Botond, et al. "β-Amyloid and the Pathomechanisms of Alzheimer’S Disease: A Comprehensive View." Molecules, vol. 22, no. 10, 2017, p.
13. Miyashita A, Koike A, Jun G, et al. SORL1 is genetically associated with late-onset Alzheimer's disease in Japanese, Koreans and Caucasians. PLoS One. 2013;8:e58618.
14. Liu G, Wang H, Liu J, et al. The CLU gene rs11136000 variant is significantly associated with Alzheimer's disease in Caucasian and Asian populations. Neuromolecular Med. 2014;16:52–60.
15. Yu JT, Ma XY, Wang YL, et al. Genetic variation in clusterin gene and Alzheimer's disease risk in Han Chinese. Neurobiol Aging. 2013;34:1921. e17–23.