Comparison of Blood Lead Levels in Patients With Alzheimer’s Disease and Healthy People

Fathabadi, B; Dehghanifiroozabadi, Mohammad; Aaseth, Jan; Sharifzadeh, Gholamreza; Nakhaee, Samaneh; Sanati, Ali Rajabpour; Amirabadizadeh, Alireza; Mehrpour, Omid

doi:10.1177/1533317518794032

Cited by 39 publications

(18 citation statements)

References 49 publications

(82 reference statements)

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“…Lead in biological systems is a neurotoxicant and a risk factor for neurodegenerative diseases (47). The signi cantly elevated blood lead levels (BLL) observed in AD patients in this study was consistent with ndings of a similar study (48). Environmental exposure to pollutants has been reported as veritable source of Lead contamination (49); hence, the elevated BLL observed in AD patients in this study may be attributed to the higher proportion of AD patients living in low-income residential areas/slums (88.9%) and/or with houses closer to tarred roads (50%) than in the controls.…”

Section: Discussionsupporting

confidence: 91%

Oxidative Stress, Trace and Toxic Metal Levels In Alzheimer’S Disease In Sub-Sahara Africa

Omotosho

Ngwube

Abdumalik

2020

Preprint

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BackgroundAlzheimer’s disease (AD), an age-related neurodegenerative disease characterized by loss of memory has been attributed to oxidative stress induced by accumulation of Amyloid (Aβ) protein 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.MethodIn this case-control study, a total of 38 participants (aged ≥ 60 years) 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.ResultsMean 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 ± 2.10 µg/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).DiscussionThe low plasma Zn coupled with high blood Pb and 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.ConclusionThe damaging effect of increasing toxic metal levels may be accentuating development of oxidative stress facilitating the progression of AD.

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Section: Discussionsupporting

confidence: 91%

Oxidative Stress, Trace and Toxic Metal Levels In Alzheimer’S Disease In Sub-Sahara Africa

Omotosho

Ngwube

Abdumalik

2020

Preprint

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“…Human epidemiological studies have showed that circulating levels of certain heavy metals are higher in patients with Alzheimer's disease than in control patients (Fathabadi et al 2018;Xu et al 2018). This suggests a potential role of heavy metals in Alzheimer's disease, but it is not yet clear whether they interfere in the development or the progression of the disease.…”

Section: Introductionmentioning

confidence: 99%

Fungicide Residues Exposure and β-amyloid Aggregation in a Mouse Model of Alzheimer’s Disease

Lafon

Wang

Arango-Lievano

et al. 2020

Environ Health Perspect

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BACKGROUND: Pesticide residues have contaminated our environment and nutrition over the last century. Although these compounds are present at very low concentrations, their long-term effects on human health is of concern. The link between pesticide residues and Alzheimer's disease is not clear and difficult to establish. To date, no in vivo experiments have yet modeled the impact of this chronic contamination on neurodegenerative disorders. OBJECTIVES: We investigated the impact of fungicide residues on the pathological markers of Alzheimer's disease in a transgenic mouse model. METHODS: Transgenic (J20, hAPP Sw=Ind) mice were chronically exposed to a cocktail of residues of cyprodinil, mepanipyrim, and pyrimethanil at 0:1 lg=L in their drinking water for 9 months. We assessed the effects of fungicide residues on the pathological markers of the disease including Ab aggregates, neuroinflammation, and neuronal loss. Then, we studied the dynamics of Ab aggregation in vivo via a longitudinal study using twophoton microscopy. Finally, we investigated the molecular mechanisms involved in the production and clearance of Ab peptides. RESULTS: We found that a chronic exposure to three fungicide residues exacerbated aggregation, microgliosis, and neuronal loss. These fungicides also increased vascular amyloid aggregates reminiscent of cerebral amyloid angiopathy between 6 and 9 months of treatment. The mechanism of action revealed that fungicides promoted Ab peptide fibril formation in vitro and involved an in vivo overexpression of the levels of the b-secretasecleaving enzyme (BACE1) combined with impairment of Ab clearance through neprylisin (NEP). CONCLUSIONS: Chronic exposure of the J20 mouse model of Alzheimer's disease to a cocktail of fungicides, at the regulatory concentration allowed in tap water (0:1 lg=L), strengthened the preexisting pathological markers: neuroinflammation, Ab aggregation, and APP b-processing. We hypothesize prevention strategies toward pesticide long-term exposure may be an alternative to counterbalance the lack of treatment and to slow down the worldwide Alzheimer's epidemic.

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“…The main sources of lead‐associated hazards include the battery industry, radiator‐related occupations, ceramics, plumbing, paint industry, cable manufacturing, and exposure to contaminated soil, contaminated foods and, in some parts of the world, opium addiction. Lead can enter the body and cause poisoning upon contact, swallowing or inhaling from any of these sources . According to the recent definitions by the United States (US) Centers for Disease Control and Prevention and National Institute of Occupational Safety and Health (NIOSH), blood lead levels (BLLs) equal to or greater than 5 μg/dL are considered as to be elevated in adults.…”

Section: Introductionmentioning

confidence: 99%

Impact of chronic lead exposure on liver and kidney function and haematologic parameters

Nakhaee

Amirabadizadeh

Brent

et al. 2018

Basic Clin Pharma Tox

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Background: Lead, one of the most widely used metals because of its beneficial physical properties, has been reported to adversely influence several different organs and organ systems. The aim of the present study was to examine the effect of lead exposure on liver and renal function and haematologic parameters. Methods: This was a case-cohort study comparing adults with occupational, environmental or opium-related lead exposure with blood lead levels [BLL] >10 μg/ dL (High blood lead level (HBLL) group and age-and gender-matched normal healthy individuals (Low blood lead level [LBLL] group with BLL <10 μg/dL). The complete blood count and concentrations of serum creatinine, urea, aspartate aminotransferase (AST), alanine aminotransferase (ALT) were recorded for subsequent investigation. Results: The mean BLL was significantly higher in the HBLL than in the LBLL groups (51.36 ± 44.72 vs 4.17 ± 1.97 µg/dL). The Spearman's rho revealed a significant association between BLL and urea (r = 0.25, P < 0.001), creatinine (r = 0.16, P = 0.02), AST (r = 0.42, P < 0.001) and ALT (r = 0.27, P < 0.001). The median [IQR] serum urea (34 mg/dL [27-221]) vs (30 [27-36]), creatinine (0.9 mg/dL [0.8-1]) vs (0.8 [0.7-0.9]), ALT (25 mg/dL [16-49]) vs (22 [16-30]) and AST concentrations (29 mg/dL [20-42]) vs (20 [18-24]) were all significantly higher (P < 0.05) in the HBLL group compared to the LBLL group.The median ]) vs (15.2 [14.6-16.3] and haematocrit (36.9% [31-44.8]) vs (45.6 [43.6-48.2]) were both significantly lower (P < 0.001) in the HBLL group than in the LBLL group. Conclusion: The results indicated that people with chronic lead exposure with BLLs greater than 10 μg/dL are at risk of renal, liver and haematologic impairments.

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Comparison of Blood Lead Levels in Patients With Alzheimer’s Disease and Healthy People

Abstract: In the present study, BLL was associated with AD.

Cited by 39 publications

References 49 publications

Oxidative Stress, Trace and Toxic Metal Levels In Alzheimer’S Disease In Sub-Sahara Africa

Oxidative Stress, Trace and Toxic Metal Levels In Alzheimer’S Disease In Sub-Sahara Africa

Fungicide Residues Exposure and β-amyloid Aggregation in a Mouse Model of Alzheimer’s Disease

Impact of chronic lead exposure on liver and kidney function and haematologic parameters

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