Help required pls! (schizophrenia).
Question:
*How many of them?
*Is bipolar disease the same with schizophrenia?
Answers:
Not an easy question to answer! Bottom line is genes play an important but not decisive role in getting a mental illness. There are mutations or changes in DNA that can lead to an increased chance of getting a mental illness.
Genes are not destiny, though. No mutations that I know of give you a 100% chance of having a mental illness. So the environment plays a critical role as well.
Let's look at schizophrenia as an example. Schizophrenia affects over 2 million Americans, around 1% of the population. And studies have shown that it clearly runs in families.
So if schizophrenia runs in the family, genes must be involved, right? Not necessarily.
Let’s use an example to show how someone might be fooled by something running in the family. Imagine there is a family that lives near a toxic waste dump. The whole family has high rates of cancer.
Is it because of their genes? Probably not. The cancer is probably the toxic waste dump’s fault, not the family’s genes.
To try to figure out what role genes play, scientists often do a twin study. Twin studies look at how often identical twins both have something compared to fraternal twins.
If something happens more often for both twins in an identical twin pair, then genes are involved. Why? Because identical twins share the exact same DNA.
The twin studies showed that if one identical twin has schizophrenia, then there is a 30-50% chance that the other twin will have it as well. If a fraternal twin has schizophrenia, then there is a 15% chance that the other twin will have it as well. (This is the same percentage as any brother and sister.)
So these results suggest that genes probably play a role. Of course genes aren’t the whole story. If they were, when one identical twin had schizophrenia, there would be a 100% chance that the other twin would have it as well.
But how might genes play a role in schizophrenia? To understand this, we need to understand a bit how the brain works and what goes wrong in mental illness.
We collect lots of information about the world with our five senses. Too much. Special brain chemicals called neurotransmitters let us sort out and make sense of these signals. If something goes wrong with this system, then you can get a mental illness.
These neurotransmitters don’t exist in a vacuum. For them to have an effect, they interact with other proteins called receptors. These receptors then cause all sorts of things to happen which then results in, for example, recognizing your mother’s voice. Mental illness can happen if something goes wrong with any of these parts.
Let’s look at a common symptom of schizophrenia, hallucinations. Normally when we see something, the brain interprets what we see with these neurotransmitters. If the neurotransmitters were to go into action without the visual cue, you’d “see” something that isn’t there. Or if the receptor fired on its own, you’d get the same result.
Great theory but have any actual genes been found? One promising gene is the glutamate receptor gene (GRM3). One of the glutamate receptor's jobs is to respond to those neurotransmitters we talked about earlier. If it responds inappropriately, then you might have the beginnings of schizophrenia.
This mutant gene is almost certainly not the whole story. If it were, we could just track it in families and see who gets schizophrenia. But there are almost certainly lots more genes involved and scientists are busily trying to find them.
And let’s not forget the environment. Because both twins in an identical twin pair didn't always get schizophrenia, the environment plays a role too. What the triggers are is still unknown. But whatever these triggers are, they play a critical role in mental illness.
Other mental illnesses are similarly complicated. By figuring out the genes involved, we can gain a greater understanding of how our brains work. And hopefully come up with better and more specific medicines to treat various mental illnesses.
There are still many researches going on, on this subject; If you like the info on research studies,hjere it is:
Although the importance of genetic factors and the distinctness from manic-depressive psychosis are indicated by twin studies, the mode of inheritance is unclear. Some (e.g., Garrone, 1962) suggested recessive inheritance. Others (e.g., Book, 1953; Slater, 1958) favored irregular dominant inheritance. A priori, polygenic inheritance seems most likely, according to the rule that relatively frequent disorders such as this do not have simple monomeric genetic determination. Within the larger group, there may be entities that behave in a simple mendelian manner. Heston (1970) reviewed the evidence and concluded that it supports the autosomal dominant hypothesis. He pointed out that the definition of schizophrenia used by researchers is a broad one encompassing the schizoid state, the 'schizophrenic spectrum.' Schizoids and schizophrenics occur with about equal frequency among the cotwins of schizophrenic monozygotic twin probands, bringing the concordance rate close to 100%. About 45% of sibs, parents, and offspring of schizophrenics are schizoid or schizophrenic, as are about 66% of the children of 2 schizophrenic parents. About 4% of the general population is affected with schizoid-schizophrenic disease. See editorial review in Lancet (Anonymous, 1970). Kidd and Cavalli-Sforza (1973) favored recessive inheritance.
Risch and Baron (1984) concluded that either a polygenic or a mixed model (with a single major locus making a major contribution to genetic liability) gives good agreement with segregation analysis of family data and is consistent with supplementary observations (lifetime disease incidences, mating-type distribution, and monozygotic twin concordance). For a polygenic model, the estimated components of variance were polygenes (H), 81.9%; common sib environment (B), 6.9%; and random environment (R), 11.2%. They concluded that in the mixed model the postulated single locus is more likely to be recessive than dominant, with a high frequency and low penetrance. The most likely recessive mixed model gave the following partition of liability variance: major locus, 62.9%; polygenes, 19.5%; common sib environment, 6.6%; and random environment, 11%. Murray et al. (1985) reviewed genetic studies of schizophrenia and suggested heterogeneity. They stated that familial cases will be the most valuable for molecular genetic study. Consideration of pooled Western European studies led to an estimate of either 2 or 3 epistatic loci (Risch, 1990).
Stober et al. (1995) conducted a family study of 139 probands who met DSM-III-R catatonic schizophrenia conditions and 543 first-degree relatives. They found an age-corrected morbidity risk of 4.6% in systematic catatonia and 26.9% age-corrected morbidity risk in periodic catatonia. They contended that this pointed strongly to a major gene effect in periodic catatonia.
Stober et al. (1995) performed a pairwise comparison of age of onset between affected probands and parents that demonstrated anticipation which was even more strikingly apparent in pedigrees with 3 successive generations affected. They suggested that there may be a major gene with trinucleotide repeat expansions or other repetitive elements affecting gene expression responsible for many cases of periodic catatonia. See also SCZD1 (181510).
Bassett and Husted (1997) noted several studies that observed anticipation (earlier age at onset in successive generations) in familial schizophrenia (Bassett and Honer, 1994; Asherson et al., 1994). In 1944, while he was working in Ontario because of his status as a conscientious objector during World War II, Lionel S. Penrose collected anticipation data on a large, representative sample of familial mental illness, using a broad ascertainment strategy (Penrose, 1991). Bassett and Husted (1997) used these data to examine anticipation and ascertainment biases in five 2-generation samples of affected relative pairs. The median intergenerational difference (MID) in age at onset was used to assess anticipation. Results showed significant anticipation in parent-offspring pairs with schizophrenia and in a positive control sample with Huntington disease (143100). Broadening the diagnosis of the schizophrenia sample suggested anticipation of severity of illness. However, other analyses provided evidence for ascertainment bias, especially in later-age-at-onset parents, in parent-offspring pairs. Aunt/uncle-niece/nephew schizophrenia pairs showed anticipation, but the MID was 8 years and aunts/uncles had earlier median age at onset than parents. Bassett and Husted (1997) interpreted the findings as suggesting that although the effects of ascertainment bias were observed in parent-offspring pairs, true anticipation appears to be inherent in the transmission of familial schizophrenia. The findings supported investigations of unstable mutations and other mechanisms that might contribute to true anticipation in schizophrenia.
Rh incompatibility had been implicated as a risk factor for schizophrenia. Hollister et al. (1996) found that the proportion of Rh-incompatible male offspring (2.1%) was significantly larger than the proportion of Rh-compatible male offspring (0.8%), yielding a relative risk of 2.78. Palmer et al. (2002) assessed the role of maternal-fetal genotype incompatibility at the RHD locus (111680) in schizophrenia. They sought to determine whether the effect of the RHD locus results from a maternal-fetal genotype incompatibility, from linkage and association with a high-risk susceptibility allele at or near the RHD locus, or from the effects of the maternal genotype acting alone. They studied 88 patient-parent trios, 72 patient-mother pairs, and 21 patient-father pairs with genotyping at the RHD locus. There was significant evidence for an RHD maternal-fetal genotype incompatibility. There was no evidence to support linkage/association with schizophrenia at or near the RHD locus and no evidence to support the role of maternal genotype effect alone.
CYTOGENETICS
Chodirker et al. (1987) reported a family in which the karyotypes of 4 brothers demonstrated a fragile site at 19p13. Two of the brothers had schizophrenia, 1 had mental retardation with autistic behavior, and 1 was phenotypically normal.
See dopamine receptor D2 (DRD2; 126450) for a description of chromosomal abnormalities of 11q associated with schizophrenia.
Kamnasaran et al. (2003) reported a mother and daughter with schizophrenia who were carriers of a t(9;14)(q34;q13) chromosome. No genes were disrupted at the breakpoint on chromosome 9, but the breakpoint on chromosome 14q12 occurred within intron 3 of the NPAS3 gene (609430), affecting the coding region of both alternative transcripts. The daughter, who was more severely affected, also had microdeletions within intron 2 of the NPAS3 gene and within intron 3 of a proximal gene, KIAA0391 (609947). Both of these intronic regions contain several possible transcription factor-binding sites
MAPPING
Linkage Studies for Complex Traits
Elston et al. (1973) attempted to demonstrate the operation of single genes through linkage studies. Feder et al. (1985) used 2 approaches to test the possible implication of the POMC gene on chromosome 2p in schizophrenia and bipolar affective illness. Both yielded negative results. The first method involved testing normal controls and patients with a variety of restriction enzymes to detect a difference due to a single nucleotide substitution that is directly responsible for the disease state. The second approach, using linkage disequilibrium, made use of DNA polymorphisms so close to the POMC gene that association would be found if a POMC mutation were responsible for all or many of the cases of either psychiatric disease. The use of the DNA markers for linkage in specific pedigrees is limited by the low penetrance and uncertain mode of inheritance.
Other Answers:
If you think your succeptable to schizophrenia, you may want to talk to your doctor. If you attempt to "self-diagnose" you might end up doing it wrong and might cause yourself more harm. Either by scaring yourself thinking you have it, or you might show early signs and might ignore them. Just consult your doctor, that's the only safe answer I can give you.
I'm scizophrenic.
And so am I. There's some research that shows how schizophrenia is linked to a gene that regulates the neurotransmitter, dopamine.
http://www.nimh.nih.gov/press/schizcompt.cfm
Previous genetic studies have identified two genes as schizophrenia risk genes—Disrupted-in- Schizophrenia 1 (DISC1) and neuregulin 1.
http://www.nimh.nih.gov/press/schizgene-workings.cfm
They have also found that children that are missing part of a particular chromosome are 30x more likely to develop schizophrenia.
http://www.nimh.nih.gov/press/comtdeletion.cfm
As far as the specific number of genes that may cause schizophrenia, I don't know. Genetic research, compared to other medicine and research, is still in its infancy and it could be decades before we identify every gene responsible for schizophrenia.
Bipolar Disorder is different from schizophrenia. Bipolar is characterized by highs (mania) and lows (depression), while schizophrenia is characterized by hallucinations, delusions, disordered thinking, social difficulties, and flat affect. However, there is an overlap. People with Bipolar Disorder can have psychotic features and people with symptoms of schizophrenia can have bipolar symptoms (Schizoaffective Disorder, Bipolar Type).
Some of the same atypical antipsychotics are used to treat mania and schizophrenia (Zyprexa, Seroquel, Risperdal, Geodon).
More Questions and Answers
- i can turn my head 360deg is this normal?
- Voices in my head?
- Lexapro for Anxiety?
- Does anyone else here cut themself?
- What is your favorite dream, you know the kind that makes you wake up and stretch and sigh and just starts?
- Why can I not move when I wake up?
- I sometimes accidentally say a displayed number incorrectly. Why?
- crazy hobo's?