ausblenden:
Schlagwörter:
EARLY-LIFE STRESS; HIGH-FAT-DIET; ADULT PSYCHIATRIC-DISORDERS;
HYPOTHALAMIC POMC PROMOTER; PITUITARY-ADRENAL AXIS; DNA METHYLATION;
GLUCOCORTICOID-RECEPTOR; PERICONCEPTIONAL UNDERNUTRITION; CHILDHOOD
ADVERSITIES; MATERNAL OBESITY; Genetics & Heredity; Neurosciences & Neurology; Psychiatry;
Zusammenfassung:
Early brain development is highly plastic due to rapid changes in cell numbers and neural connectivity that together allow the integration of a broad scope of intrinsic and environmental cues important to normal function and the risk for future disease. While cellular mechanisms are well-known for their role in neuronal plasticity, molecular epigenetic mechanisms, notably DNA methylation and posttranslational histone modifications, have emerged only recently. Epigenetic marking can serve to inscribe environmental experiences at the level of the DNA and chromatin and thus generate long-lasting, though potentially reversible, memory traces of the past. Here, we will review the developmental, physiological, and molecular framework by which psychological, social, and nutritional cues are thought to impact on the epigenome of neuronal cells with a role in stress regulation and how such epigenetic marks can give rise to long-lasting adaptations that represent major risk factors for distinct neuropsychiatric diseases.
