Heavy Metals Exposure and Alzheimer’s Disease and Related Dementias

Bakulski, Kelly M.; Seo, Young Ah; Hickman, Ruby C; Brandt, Daniel; Vadari, Harita S; Hu, Howard; Park, Sung Kyun

doi:10.3233/jad-200282

Cited by 187 publications

(201 citation statements)

References 209 publications

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“…However, most of these associations are only epidemiological, and more studies are necessary to understand the role of Pb in the pathophysiology of these disorders [ 107 ]. On the other hand, although there is evidence that chronic Pb poisoning seems to be related to decreased cognitive performance, there are still no formal longitudinal epidemiological studies that demonstrate an association between previous exposure to Pb and the future risk of developing Alzheimer’s disease or other dementias, but experimental studies seem to show that multiple mechanisms of damage are common between Pb-neurotoxicity and Alzheimer’s disease [ 108 ].…”

Section: Lead Exposure During Developing Brain Early Life and Admentioning

confidence: 99%

Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead Neurotoxicity

Ortega

González-Esquivel

Ayala

et al. 2021

Toxics

107

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Lead (Pb) is considered a strong environmental toxin with human health repercussions. Due to its widespread use and the number of people potentially exposed to different sources of this heavy metal, Pb intoxication is recognized as a public health problem in many countries. Exposure to Pb can occur through ingestion, inhalation, dermal, and transplacental routes. The magnitude of its effects depends on several toxicity conditions: lead speciation, doses, time, and age of exposure, among others. It has been demonstrated that Pb exposure induces stronger effects during early life. The central nervous system is especially vulnerable to Pb toxicity; Pb exposure is linked to cognitive impairment, executive function alterations, abnormal social behavior, and fine motor control perturbations. This review aims to provide a general view of the cognitive consequences associated with Pb exposure during early life as well as during adulthood. Additionally, it describes the neurotoxic mechanisms associated with cognitive impairment induced by Pb, which include neurochemical, molecular, and morphological changes that jointly could have a synergic effect on the cognitive performance.

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Section: Lead Exposure During Developing Brain Early Life and Admentioning

confidence: 99%

Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead Neurotoxicity

Ortega

González-Esquivel

Ayala

et al. 2021

Toxics

107

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“…While acute exposures to HMs knowingly causes severe toxic effects, concerns by public health authorities are currently focused on chronic, low-dose exposures, which can lead to cumulative effects. Even exposures to HMs at levels lower than those assigned for “safe” threshold values are potentially toxic, resulting in cancer, neurological damage, and infertility, among other effects [ 220 , 221 , 222 ].…”

Section: Cellular and Molecular Mechanisms Of Toxicity On Hematopomentioning

confidence: 99%

Cellular and Molecular Mechanisms of Environmental Pollutants on Hematopoiesis

Scharf

Broering

Rocha

et al. 2020

IJMS

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Hematopoiesis is a complex and intricate process that aims to replenish blood components in a constant fashion. It is orchestrated mostly by hematopoietic progenitor cells (hematopoietic stem cells (HSCs)) that are capable of self-renewal and differentiation. These cells can originate other cell subtypes that are responsible for maintaining vital functions, mediate innate and adaptive immune responses, provide tissues with oxygen, and control coagulation. Hematopoiesis in adults takes place in the bone marrow, which is endowed with an extensive vasculature conferring an intense flow of cells. A myriad of cell subtypes can be found in the bone marrow at different levels of activation, being also under constant action of an extensive amount of diverse chemical mediators and enzymatic systems. Bone marrow platelets, mature erythrocytes and leukocytes are delivered into the bloodstream readily available to meet body demands. Leukocytes circulate and reach different tissues, returning or not returning to the bloodstream. Senescent leukocytes, specially granulocytes, return to the bone marrow to be phagocytized by macrophages, restarting granulopoiesis. The constant high production and delivery of cells into the bloodstream, alongside the fact that blood cells can also circulate between tissues, makes the hematopoietic system a prime target for toxic agents to act upon, making the understanding of the bone marrow microenvironment vital for both toxicological sciences and risk assessment. Environmental and occupational pollutants, therapeutic molecules, drugs of abuse, and even nutritional status can directly affect progenitor cells at their differentiation and maturation stages, altering behavior and function of blood compounds and resulting in impaired immune responses, anemias, leukemias, and blood coagulation disturbances. This review aims to describe the most recently investigated molecular and cellular toxicity mechanisms of current major environmental pollutants on hematopoiesis in the bone marrow.

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“…Noteworthy, most AD cases are sporadic in nature and influenced by a range of genetic and environmental factors. Recent epidemiological studies suggest an association of Pb burden and AD dementia (reviewed in [ 107 , 108 ]). Childhood Pb exposure, particularly in the critical period, leads to permanent alterations in nervous system functions, and this might extend to predisposing the brain to ageing-induced neurodegeneration, such as AD [ 109 ].…”

Section: Pb Neurotoxicity In Childrenmentioning

confidence: 99%

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

Ahmad

Liu

2020

Antioxidants

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Lead (Pb) neurotoxicity is a major concern, particularly in children. Developmental exposure to Pb can alter neurodevelopmental trajectory and has permanent neuropathological consequences, including an increased vulnerability to further stressors. Ascorbic acid is among most researched antioxidant nutrients and has a special role in maintaining redox homeostasis in physiological and physio-pathological brain states. Furthermore, because of its capacity to chelate metal ions, ascorbic acid may particularly serve as a potent therapeutic agent in Pb poisoning. The present review first discusses the major consequences of Pb exposure in children and then proceeds to present evidence from human and animal studies for ascorbic acid as an efficient ameliorative supplemental nutrient in Pb poisoning, with a particular focus on developmental Pb neurotoxicity. In doing so, it is hoped that there is a revitalization for further research on understanding the brain functions of this essential, safe, and readily available vitamin in physiological states, as well to justify and establish it as an effective neuroprotective and modulatory factor in the pathologies of the nervous system, including developmental neuropathologies.

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Heavy Metals Exposure and Alzheimer’s Disease and Related Dementias

Cited by 187 publications

References 209 publications

Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead Neurotoxicity

Cognitive Impairment Induced by Lead Exposure during Lifespan: Mechanisms of Lead Neurotoxicity

Cellular and Molecular Mechanisms of Environmental Pollutants on Hematopoiesis

(Ascorb)ing Pb Neurotoxicity in the Developing Brain

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