Journal of Alzheimers Disease & Parkinsonism
Open Access

Oxidative Stress, Trace and Toxic Metal Levels in Alzheimer’s Disease in Sub-Sahara Africa

Ishiaq Olayinka Omotosho^1*, Michael Roland Ngwube¹ and Jibril Omuya AbdulMalik²

¹Department of Chemical Pathology, College of Medicine, University of Ibadan, Nigeria

²Department of Psychiatry, College of Medicine, University of Ibadan, Nigeria

Received Date: Jan 02, 2023 / Published Date: Jan 31, 2023

Citation: Omotosho IO, Ngwube MR, AbdulMalik JO (2023) Oxidative Stress, Trace and Toxic Metal Levels in Alzheimer’s Disease in Sub-Sahara Africa. J Alzheimers Dis Parkinsonism. 13:561.DOI: 10.4172/2161-0460.1000561

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Copyright: © 2023 Omotosho IO, et al. This is an open-access article distributed under the terms of the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

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Background: Alzheimer’s Disease (AD), an age-related neurodegenerative disease characterized by loss of memory has been attributed to oxidative stress induced by accumulation of Amyloid Protein (Aβ) in the brain; environmental and genetic alterations have been implicated as the pathogenesis of the disease. This work investigated levels of selected trace (Iron, Zinc and Copper) and toxic (Cadmium and Lead) metals in AD patients.

Method: In this case-control study, a total of 38 participants (aged>60years) consisting of 18 clinically diagnosed AD subjects and 20 apparently healthy age-matched adults were recruited from the University College Hospital Ibadan Geriatric Centre. Semi-structured questionnaire was used to obtain demographic information, clinical history, lifestyle and dietary patterns from participants. Blood levels of iron, copper, zinc, lead and cadmium were analyzed using Atomic Absorption Spectrophotometry (AAS); levels of Malondialdehyde (MDA), Total Antioxidant Capacity (TAC), Hydrogen Peroxide (H₂O₂), and Total Plasma Peroxide (TPP) were determined spectrophotometrically, while Oxidative Stress Index (OSI) and copper to zinc ratio (Cu:Zn) were calculated.

Results: Mean plasma level of zinc was significantly lower in cases (86.04 ± 11.07 µg/dl) compared to controls (108.80 ± 12.47 µg/dl), while blood lead (13.85 ± 2.96 µg/dl, 8.32 ± 2.10µg/dl) and cadmium (1.34 ± 0.71 µg/L, 0.71 ± 0.14 µg/L) levels were significantly higher in cases than in controls respectively. Although Fe and Cu levels were similar in cases and controls, Cu:Zn ratio was significantly elevated in cases compared to controls (p=0.000). Though other OS markers were not significantly different in both groups, TPP was significantly higher in cases [64.96 ± 7.20 µmol/ H₂O₂ vs. 55.41 ± 2.38 µmol/H₂O₂) while MDA correlated inversely with TAC in cases (r= -0.477, p=0.045).

Discussion: The low plasma Zn coupled with high blood Lead (Pb) and Cadmium (Cd) levels may precipitate the elevated TPP and Cu:Zn ratio in cases. The reduced metallothionine defense of the system as indicated by the elevated Cu:Zn ratio in cases may also exacerbate this problem.

Conclusion: The damaging effect of increasing toxic metal levels may be accentuating development of oxidative stress facilitating the progression of AD.

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