心理学と精神医学: オープンアクセス

抽象的な

Auto-inflammation is a Diaeventontological Trigger in Neuropsychiatric disorders

Daniel J Guerra

Single biochemical or cellular events cannot be expected to explain complex neuropsychiatric disease and, while animal models are indispensable for pharmacotherapy and pharmaceutical discovery, they will not fully apprehend these human disorders. Clinical studies have the advantage of authentic examination of human neuropsychiatric pathology, but they cannot holistically arrive at sound theories or practice for surmounting these debilitating diseases, even when precise molecular tools are employed. This is because ‘Systems’ approaches such as the standard OMIX platforms or cell Sorting/Screening from biological specimens fail to imagine the three-dimensional architectonics of Genetic Environmental and Neuroimmunoepigentic phenomena as event ontologies through time. The distinction is based on arrangement of a recombining between the phenomenological and the metaphysical states appropriated from neuropsychiatric diagnosis from the existing individual perspective rather than externally, as if from a static organization into categories of pathophysiology as outlined in the DSM. This turn to the individual diagnosis,allows for the fusion of event ontologies with the personal experiences of the existing individual. This is how the immune system integrates neurophysiological states with neuropsychiatric disease.The immune system encounters perpetual modifications of the stress-laden environment and most of these cellular and signal tranducing cascades of biochemical pathway alterations are subsumed in transcriptionl and post-translational molecular events.