in nonessential heavy metal concentrations in air, water and food sources, and household products has increased the risk of chronic exposure. acetylation, methylation and histone modification are some of the most common epigenetic markers. while these changes do not directly affect the dna sequence, they are able to alter the accessibility to genetic components, such as the promoter or enhancer regions, necessary for gene expression. studies have shown that long-term maternal exposure to lead (pb) contributes to decreased methylation in areas of the fetal epigenome, for example the interspaced repetitive sequences (irss) alu1 and line-1. the hypomethylation of these irss has been linked to increased risk for cancers and autoimmune diseases later in life. additionally, studies have found a relationship between chronic prenatal pb exposure and neurological diseases, such as alzheimer's and schizophrenia, as well as developmental issues. furthermore, the acetylation and methylation changes induced by overexposure to lead result in decreased neurogenesis and neuron differentiation ability, and consequently interfere with early brain development. overexposure to essential metals can also have detrimental consequences on the epigenome. for example, when manganese, a metal normally used by the body as a cofactor, is present at high concentrations in the blood it can negatively affect the central nervous system. studies have shown that accumulation of manganese leads to dopaminergic cell death and consequently plays a role in the onset of parkinson's disease (pd). a hallmark of parkinson's disease is the accumulation of α-synuclein in the brain. increased exposure to manganese leads to the downregulation of protein kinase c delta (pkcδ) through decreased acetylation and results in the misfolding of the α-synuclein protein that allows aggregation and triggers apoptosis of dopaminergic cells. research the field has only recently seen a growth in interest, as well as in research, due to technological advancements that facilitate better resolution of the minute modifications made to dna. however, even with the significant advances in technology, studying the biology of neurological phenomena, such as cognition and addiction, comes with its own set of challenges. biological study of cognitive processes, especially with humans, has many ethical caveats. some procedures, such as brain biopsies of rett syndrome patients, usually call for a fresh tissue sample that can only be extricated from the brain of deceased individual. in such cases, the researchers have no control over the age of brain tissue sample, thereby limiting research options. in case of addiction to substances such as alcohol, researchers utilize mouse models to mirror the human version of the disease. however, the mouse models are administered greater volumes of ethanol than humans normally consume in order to obtain more prominent phenotypes. therefore, while the model organism and the tissue samples provide an accurate approximation of the biology of neurological phenomena, these approaches do not provide a complete and precise picture of the exact processes underlying a phenotype or a disease. neuroepigenetics had also remained underdeveloped due to the controversy surrounding the classification of genetic modifications in matured neurons as epigenetic phenomena. this discussion arises due to the fact that neurons do not undergo mitosis after maturation, yet the conventional definition of epigenetic phenomena emphasizes heritable changes passed on from parent to offspring. however, various histone modifications are placed by epigenetic modifiers such as dna methyltransferases (dnmt) in neurons and these marks regulate gene expression throughout the life span of the neuron. the modifications heavily influence gene expression and arrangement of synapses within the brain. finally, although not inherited, most of these marks are maintained throughout the life of the cell once they are placed on chromatin.