The disease model of addiction describes an addiction as a disease with genetic, biological, neurological or environmental origin.[1] The traditional medical model of disease requires only an abnormal condition causing distress, discomfort or dysfunction to an affected individual. The contemporary medical model partly attributes addiction to changes in the brain's mesolimbic pathway.[2] The model also considers these diseases as a result of other biological, psychological or sociological entities, despite an incomplete understanding of their mechanisms. The common biomolecular mechanisms underlying addiction – CREB and ΔFosB – were reviewed by Eric J. Nestler in a 2013 review.[3] Genetics and mental disorders may precipitate the severity of a drug addiction. It is estimated that 50% of healthy individuals developing an addiction can trace the cause to genetic factors.[4]
Despite the importance of numerous psychosocial factors, at its core, drug addiction involves a biological process: the ability of repeated exposure to a drug of abuse to induce changes in a vulnerable brain that drive the compulsive seeking and taking of drugs, and loss of control over drug use, that define a state of addiction. Here, we review the types of molecular and cellular adaptations that occur in specific brain regions to mediate addiction-associated behavioral abnormalities. These include alterations in gene expression achieved in part via epigenetic mechanisms, plasticity in the neurophysiological functioning of neurons and synapses, and associated plasticity in neuronal and synaptic morphology mediated in part by altered neurotrophic factor signaling. [emphasis in original]