If the present hypothesis is supported at the molecular level, it would likely force a foundational shift in how the neurobiology of common forms of psychopathology is conceptualized. Genetic polymorphisms influence risk for psychopathology by encoding protein components of neurons and other relevant biological systems through a chain of processes. If many genetic polymorphisms are pleiotropically associated with variation in all psychopathology dimensions (and within the internalizing and externalizing domains) that would almost certainly mean that those correlated forms of psychopathology share many aspects of their genetically influenced pathophysiology. That is, in contrast to the dominant paradigm in which forms of psychopathology are studied singly as if each were neurobiologically unique, the present genetic hypothesis implies that patterns of dysfunction in neurobiological systems may be related to risk for multiple psychopathology dimensions, likely through transactions with the environment. In turn, this implies that neurobiological studies should consider both multiple neurobiological systems and multiple forms of psychopathology at the same time to identify both the common and dimension-specific mechanisms underlying psychopathology.
