Abstract
The foundation for the development of a broad spectrum of stress-related disorders is laid early in development. Early-life stress, including prenatal stress exposure, increases individual susceptibility for the development of mental disorders and physical diseases across the lifespan. Persistent alterations in the brain as well as in endocrine, immune, and metabolic systems underlie this developmental programming of disease susceptibility. Thus, stress exposure in early developmental stages results in neurobiological traces or “scars” in the central nervous system that render individuals susceptible to developing a broad range of diseases throughout the lifespan. Recent evidence suggests that this risk can be passed on to subsequent generations. Genetic factors and the developmental timing of adverse exposures moderate the clinical and biological consequences of early-life stress as well as individual vulnerability to disease and course of disease. A better understanding of the neurobiological mechanisms that link exposure to early life stress with disease risk will allow for the identification of measurable parameters to help identify individuals at risk of disease and susceptibility to a specific intervention. A precise understanding of the processes of biological embedding of early life stress will further enable the development of mechanism-derived targets and time windows for interventions and prevention strategies.
Original language | English (US) |
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Title of host publication | Psychoneuroscience |
Publisher | Springer Berlin Heidelberg |
Pages | 175-190 |
Number of pages | 16 |
ISBN (Electronic) | 9783662657744 |
ISBN (Print) | 9783662657737 |
DOIs | |
State | Published - Jan 1 2023 |
All Science Journal Classification (ASJC) codes
- General Medicine
- General Neuroscience