While the proportion of mental health problems is approximately the same for younger adults, older adults are more vulnerable than younger adults to develop psychological problems resulting from factors that impact the quality of life such as stress, ill health, loss, decline in cognitive skills, and changes in living situations. The Aging Body Although aging affects everyone, its rate and extent varies from person to person. Changes in childhood and adolescence are stepwise and predictable, but advancing age means increased diversity. In the latter decades of life, people age at very different rates.
Heritability[ edit ] Evidence suggests that genetic vulnerability with environmental factors can act in combination resulting in the development of schizophrenia. Many people who appear to carry "schizophrenia genes" may not become schizophrenic.
Some twin studies   have found rates as low as The paternal age is a factor in schizophrenia because of the increased likelihood of mutations in the chromosomes of cells that produce sperms. The chance of a copying error in DNA replication during cell division increases with the number of cell divisions, and an increase in copying errors may cause an accumulation of mutations that are responsible for an increased incidence of schizophrenia.
Recently however, quite some large-scale studies have now begun to unravel the genetic underpinnings for the disease. Important segregation should be made between lower risk, common variants identified by candidate studies or genome-wide association studies GWAS and high risk, rare variants which could be caused by de novo mutations and copy-number variations CNVs.
Candidate gene studies[ edit ] An older review of linkage studies also listed seven genes as likely to increase risk for a later diagnosis of the disorder. Knockout studies in Drosophila show that reduced expression of dysbindin reduced glutamatergic synaptic transmission, resulting in impaired memory.
This female-specific association was replicated in several populations. The statistical distributions suggested nothing more than chance variation. The authors concluded that the findings make it unlikely that common SNPs in these genes account for a substantial proportion of the genetic risk for schizophrenia, although small effects could not The various causes of mental retardation ruled out.
The result showed that although the mice mostly developed normally, on further brain development, glutamate receptors broke down. This theory supports the glutamate hypothesis of schizophrenia. People normally have two copies of each gene, but in autistics some genome locations have only single copies and in schizophrenics extra copies are present at the same locations.
Distinct symptomatic subtypes of schizophrenia groups showed to have a different pattern of SNP variations, reflecting the heterogeneous nature of the disease. C4 was found to play a role in synapse pruning, and increased C4 expression leads to reduced dendritic spines and a higher schizophrenia risk.
Within them, deletions in regions related to psychosis were observed, as well as deletions on chromosome 15q This results in deletions and duplications of dosage sensitive genes. It has been speculated that CNVs underlie a significant proportion of normal human variation, including differences in cognitive, behavioral, and psychological features, and that CNVs in at least three loci can result in increased risk for schizophrenia in a few individuals.
Overlap with other disorders[ edit ] Several studies have suggested that genetic overlap exists between schizophrenia and other psychiatric disorders.
This group found four gene areas that all overlapped with the five disorders, two of which regulate calcium balance in the brain. Evolution of schizophrenia Schizophrenia has been considered an evolutionary puzzle due to the combination of high heritability, relatively high prevalence, and reduced reproductive success.
One explanation could be increased reproductive success by close relatives without symptoms but this does not seem to be the case.
Still, it has been argued that it is possible that a low amount of schizotypy increasing genes may increase reproductive success by increasing such traits such as creativity, verbal ability, and emotional sensitivity.
This is argued to be caused by an unbalanced genomic imprinting favoring paternal genes in the case of autism and maternal genes in the case of psychosis. Nevertheless, the increased average risk is well-replicated, and such events may moderate the effects of genetic or other environmental risk factors.
The specific complications or events most linked to schizophrenia, and the mechanisms of their effects, are still under examination. However, the effect is not large. Explanations have included a greater prevalence of viral infections at that time, or a greater likelihood of vitamin D deficiency.
A similar effect increased likelihood of being born in winter and spring has also been found with other, healthy populations, such as chess players. In the first and only prospective study of the low birthweight, schizophrenia, and enlargement of brain ventricles suggestive of cerebral atrophy, Leigh Silverton and colleagues found that low birthweight measured prospectively with regard to psychopathology was associated with enlarged ventricles on CT-Scans in a sample at risk for schizophrenia over 30 years later.
These signs suggestive of cerebral atrophy were associated with schizophrenia symptoms. The investigators suggested that in utero insults may specifically stress those with a schizophrenia diathesis suggesting to the authors a diathesis stress etiological model for a certain type of schizophrenia that Kraepelin identified with early abnormalities suggesting brain atrophy.Behavioral approaches help engage people in drug abuse treatment, provide incentives for them to remain abstinent, modify their attitudes and behaviors related to drug abuse, and increase their life skills to handle stressful circumstances and environmental cues that may trigger intense craving for drugs and prompt another cycle of compulsive abuse.
Caballero and Hendrich () provided a review of the role of MECP2 in the developing brain, the targets of MECP2-mediated repression, and the possible effect of misexpressed gene targets leading to clinical manifestations of RTT.
Rett Syndrome. Rett syndrome (RTT; ) is a progressive neurologic developmental disorder and one of the most common causes of mental retardation in females. Section. Category of Impairments, Mental Disorders Neurocognitive disorders Schizophrenia spectrum and other psychotic disorders.
Caballero and Hendrich () provided a review of the role of MECP2 in the developing brain, the targets of MECP2-mediated repression, and the possible effect of misexpressed gene targets leading to clinical manifestations of RTT. Rett Syndrome. Rett syndrome (RTT; ) is a progressive neurologic developmental disorder and one of the most common causes of mental retardation .
Mental Retardation. Mental retardation is defined by the American Association on Intellectual and Developmental Disabilities as “a disability characterized by significant limitations both in intellectual functioning and in adaptive behavior as expressed in conceptual, social, and practical adaptive skills” that originates before age 18 years.
The causes of schizophrenia have been the subject of much debate, with various factors proposed and discounted or modified..
The language of schizophrenia research under the medical model is scientific. Such studies suggest that genetics, prenatal development, early environment, neurobiology, and psychological and social processes are important contributory factors.