Research on epigenetic changes caused by differences in the amount of time rats were nurtured by their mother is one example of these significant impacts.
It is hypothesized that increasing cortisol levels in mothers reduces the amount of glucocorticoid receptors (GRs) in an infant's hippocampus, lowering the physiological role of the negative feedback loop on the hypothalamic-pituitary-adrenal (HPA) axis.
When the negative feedback loop is disrupted due to stress, the HPA axis in newborns becomes hyperactive and the amount of cortisol in circulation elevates.
They play a large role in a majority of physiological functions involving metabolism, blood pressure, breathing, the immune system, and behavior.
Early life exposure to stress during the critical period of childhood development can result in permanent changes to adult response systems.
These impacts are also seen at the cognitive level, causing deficits in synaptic plasticity, decreased synapse strength, an inhibited ability to form and maintain memories, and changes in mood.
[4] The circadian clock is a biochemical oscillator in organisms that is in sync with the 24 hour cycle of the Earth's rotation and has been found to impact gene expression and behavior.
This modification promotes the assembly of transcription factors via the loosening of chromatin and the ability of acetyl groups to act as binding sites.
Studies in sleep-deprived rats have found a decrease in acetylated histones at the BDNF promoter IV, which is crucial for learning and memory.
The roles of LncRNAs include regulation of splicing and translation and recruitment of epigenetic and regulatory components to target genomic loci.
The fact that a large portion of tissue-specific RNA exists in the brain is evidence that LncRNAs might play a role in neuronal function.
Insomnia may be the result of an epigenetic control process of sleep mechanics and may be influenced by changes in brain plasticity caused by exposure to stress.
[10] Current evidence indicates that histone modifications, non-coding RNAs, and DNA methylation are epigenetic mechanisms that are involved in sleep apnea.
[11] Having untreated obstructive sleep apnea can lead to developmental deficits such as cognitive impairments, hyperactivity disorder, and poor performance in academic endeavors.
[11] There are various hypoxia-mediated perturbations of gene expression that are attributed to obstructive sleep apnea comorbidities due to epigenetic mechanisms.
[14] Additionally, the critical role dopamine plays in the synaptic signals of thalamic and neocortical neurons which cause the visual and motor hallucinations in dreams is worth considering.
In one study, the use of KB200Z, a dopamine agonist, alleviated the negative symptoms of lucid nightmares in participants with histories of abuse, addiction and PTSD.
[14] Epigenetic alteration of neuroplasticity may be significantly inhibited via targeting dopamine pathways and trauma-induced deficiencies in functional connectivity.
[4] This decreased histone acetylation has been linked to learning and memory deficits and abnormalities in individuals' circadian clock.Trichostatin A has proven to be beneficial when treating sleep deprivation.
The research suggests that taking measures to reverse the epigenetic changes caused by gestational sleep fragmentation decreases the susceptibility of individuals to metabolic disorders such as diabetes and preeclampsia.
Difficulties arise when developing epigenetic treatment due to the highly-sensitive nature of the epigenome in response to the circumstances of its environment.