Biochemical mechanisms of Alzheimer's disease: Narrative Review

Iman Noori Mahmood Mahdi 1, *, Fatimah Yanadi Mohammed Ismail 2 and Nermen R. Ahmad 1

1 Department of Chemistry, College of Science, University of Kirkuk, Kirkuk, Iraq.
2 Department of Chemistry, College of Education for Women, University of Kirkuk, Kirkuk, Iraq.
Review
Open Access Research Journal of Multidisciplinary Studies, 2026, 11(02), 048-062.
Article DOI: 10.53022/oarjms.2026.11.2.0033
Publication history: 
Received on 26 February 2026; revised on 04 April 2026; accepted on 07 April 2026
 
Abstract: 
The most debilitating form of neurodegeneration in the human brain is the alzheimer disease (AD) which incurs 60-70 percent of all the diagnosed cases of dementia globally. Current biochemistry has shown that this illness is not an acute phenomenon but a silent build up of molecular imbalances that start 20 or more years prior to the emergence of symptoms. Fundamentally, Alzheimer disease is a complex tragedy of the biochemical nature when three factors come together: first, the malfunction of the processing of the amyloid precursor protein (APP), leading to the appearance of toxic A B1 42 in the cerebral spinal fluid in concentration higher than 500 nmol/L, an A B1 42/ A B 0 ratio greater than the Secondly, over-phosphorylation of tau protein on particular loci including Thr181, Thr217 and Ser202/Thr205 (epitope AT8) is indicated by high plasma p-tau 181 levels of over 2.2 pg/mL and p-tau 217 levels of over 0.37 pg/mL. Thirdly, chronic oxidative stress is indicated by elevated urinary 8-OHdG levels above 12 nmol/mmol creatinine and serum malondialdehyde levels above 4.2 nmol/mL. This article explores these interconnected biochemical mechanisms and their measurable biomarkers to provide a comprehensive picture linking molecular interactions to detectable and diagnostic biological changes.
 
Keywords: 
Alzheimer's disease; Biochemical biomarkers; Aβ42; p-tau217; Oxidative stress; 8-OHdG; Neuroinflammation; IL-1β; APOE4; GSK-3β; NfL; GFAP
 
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