Molecular Mechanisms of Lead Neurotoxicity

Dear Colleagues,

Despite the introduction of numerous preventative measures that have helped to reduce the use of lead in industry and other areas of life, its presence in the environment and toxicity rank it second among the most dangerous environmental poisons (Substance Priority List, 2018, ATSDR). Its neurotoxic effects are especially pronounced in a developing brain, and exposure in prenatal and early postnatal periods causes numerous metabolic and structural changes, resulting in neurobehavioural and cognitive disorders.

Various papers show a correlation between elevated blood levels of lead in children and impaired memory, concentration, learning, and reduced IQ levels. Recent studies also suggest the significant role of lead in the pathogenesis of neurodevelopmental disorders such as autism, schizophrenia, and ADHD. Furthermore, neurodegenerative disorders such as Alzheimer’s and Parkinson’s disease are likely to be the result not only of genetic and lifestyle factors but also of early life exposure to environmental risk factors such as lead. Although the precise mechanisms of lead neurotoxicity have not been fully described, some researchers indicate its negative influence at electrophysiological, neurobiochemical, and molecular levels.

Given the above, we would like to encourage researchers to send original papers and reviews identifying and explaining the mechanisms of the neurotoxic activity of lead, with particular emphasis on the influence of this element on neurogenesis, signal transmission pathways, synaptic protein function, synaptic transmission and plasticity, the induction and propagation of inflammation, and on astrocyte-neuron metabolic cooperation, i.e., all molecular mechanisms responsible for potential cognitive impairment and intensification of neurodegenerative processes in exposure to lead.

Prof. Dariusz Chlubek
Prof. Irena Baranowska-Bosiacka
Guest Editors

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