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Schizophrenia is a debilitating and often misunderstood disorder that affects up to 1% of the world's population. [1] Although schizophrenia is a heavily studied disorder, it has remained largely impervious to scientific understanding; epigenetics offers a new avenue for research, understanding, and treatment.
The self-domestication hypothesis for evolution of schizophrenia observes the importance our self-domesticated evolution, with emphasis on its contribution to the altered genetic development of the neural crest and our relaxed social cultural niche. Adaptations related these domesticated changes favored the emergence of complex cognitive ...
The risk of enlarged ventricles on brain scan (associated with schizophrenia symptoms and biologically suggestive of Emil Kraepelin's dementia praecox) was greatly increased if the subjects had both a higher genetic load for schizophrenia and lower birthweight. The investigators suggested that in utero insults may specifically stress those with ...
The basic principle behind psychiatric genetics is that genetic polymorphisms (as indicated by linkage to e.g. a single nucleotide polymorphism) are part of the causation of psychiatric disorders. [1] Psychiatric genetics is a somewhat new name for the old question, "Are behavioral and psychological conditions and deviations inherited?".
The causes of schizophrenia that underlie the development of schizophrenia, a psychiatric disorder, are complex and not clearly understood.A number of hypotheses including the dopamine hypothesis, and the glutamate hypothesis have been put forward in an attempt to explain the link between altered brain function and the symptoms and development of schizophrenia.
The question of how schizophrenia could be primarily genetically influenced, given that people with schizophrenia have lower fertility rates, is a paradox. It is expected that genetic variants that increase the risk of schizophrenia would be selected against, due to their negative effects on reproductive fitness .
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The glutamate hypothesis of schizophrenia models the subset of pathologic mechanisms of schizophrenia linked to glutamatergic signaling. The hypothesis was initially based on a set of clinical, neuropathological, and, later, genetic findings pointing at a hypofunction of glutamatergic signaling via NMDA receptors .
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