Will schizophrenia be cured one day? From great inventors to prodigious minds, many have suffered this disease throughout history.
Prick up your ears! Because we believe as long as tech develops, there will surely be a cure for many unsolved mysteries of medicine. How much can we use our brain or how much do we know about it? One says, we know only %8 of it, the other says %10, another says primates use just one percent less than us! Do you know that a neurosurgeon doesn’t know nearly fifty maybe more percent on why does his patients die, he might diagnose the disease but cannot cure it, cos’ our brains are enigmatic.
Well, good news, Scientists may have found a gene that links the three previously unrelated biological changes most commonly blamed for causing schizophrenia, making it one of the most promising culprits for the disease so far, and a good target for future treatments.
What is Schizophrenia?
Schizophrenia is a debilitating mental disorder that usually appears in late adolescence, and changes the way people think, act and perceive reality. For decades, scientists have struggled to work out what causes the hallucinations and strange behavior associated with the disorder, and keep coming back to three neuronal changes that seem to be to blame. The only problem is that the changes seemed to be unrelated, and, in some cases, even contradictory.
The five sub-classifications of schizophrenia according to American Psychiatric Association’s fifth edition Diagnostic and Statistical Manual of Mental Disorders (DSM-5):
Paranoid type: Delusions or auditory hallucinations are present, but thought disorder, disorganized behavior, or affective flattening are not. Delusions are persecutory and/or grandiose, but in addition to these, other themes such as jealousy, religiosity, or somatization may also be present.
John Nash, an American mathematician and joint winner of the 1994 Nobel Prize for Economics, who had schizophrenia. His life was the subject of the 2001 Academy Award-winning film A Beautiful Mind.
Disorganized type: Named hebephrenic schizophrenia in the ICD. Where thought disorder and flat affect are present together.
Catatonic type: The subject may be almost immobile or exhibit agitated, purposeless movement. Symptoms can include catatonic stupor and waxy flexibility.
Undifferentiated type: Psychotic symptoms are present but the criteria for paranoid, disorganized, or catatonic types have not been met.
Residual type: Where positive symptoms are present at a low intensity only.
; or World Health Organization’s International Statistical Classification of Diseases and Related Health Problems (ICD-10) defines two additional subtypes:
Post-schizophrenic depression: A depressive episode arising in the aftermath of a schizophrenic illness where some low-level schizophrenic symptoms may still be present.
Simple schizophrenia: Insidious and progressive development of prominent negative symptoms with no history of psychotic episodes.
According to Science Alert, Researchers from Duke University, have managed to find a link between these three hypotheses, and have shown that all three changes can be brought about by a malfunction in the same gene. Published in Nature Neuroscience, the researchers explain that their results could lead to new treatment strategies that target the underlying cause of the disease, rather than the visible changes or phenotypes, associated with schizophrenia.
In a press release, Lead Researcher Scott Soderling, a professor of cell biology and neurobiology from Duke University, says
“The most exciting part was when all the pieces of the puzzle fell together. When [co-researcher Il Hwan Kim] and I finally realised that these three outwardly unrelated phenotypes … were actually functionally interrelated with each other, that was really surprising and also very exciting for us.”
What are these three phenotypes?
The first is spine pruning, which means that the neurons of people with schizophrenia have fewer spines – the long part of a brain cell that passes signals back and forth. Some people with schizophrenia also have hyperactive neurons, and excess dopamine production.
However these changes just didn’t seem to make sense together. After all, how could neurons be overactive if they didn’t have enough dendritic spines to pass messages back and forth, and why would either of these symptoms trigger excess dopamine production? Now, researchers believe that a mutation in the gene Arp2/3 may be to blame.
Research team originally spotted the gene during previous studies, which identified thousands of genes linked to schizophrenia. But Arp2/3 was of particular interest, as it controls the formation of synapses, or links, between neurons.
In order to conceptualize its effect, the researchers engineered mice that didn’t have the Arp2/3 gene and, surprisingly, found that they behaved very similarly to humans with schizophrenia. The mice also got worse with age and improved slightly with antipsychotic medications, both traits of human schizophrenia. Above all, the most fascinating finding was the fact that the mice also had all three of the unrelated brain changes – fewer dendritic spines, overactive neurons and excess dopamine production.
This has also unearthed a big slice of the bigger picture and showed, for the first time, that this lack of dendritic spines can actually trigger hyperactive neurons. This is because the mice’s brain cells rewire themselves to bypass these spines, effectively skipping the ‘filter’ that usually keeps their activity in check. Another thread is that they also showed that these overactive neurons at the front of the brain were then stimulating other neurons to dump out dopamine.
Reporter for Medical Daily, Susan Scutti says “Overall, the combined results reveal how three separate pathologies, at the tiniest molecular level, can converge and fuel a psychiatric disorder,”
For the Full Article: http://www.medicaldaily.com/what-causes-schizophrenia-scientists-find-clues-3-different-forms-neuronal-activity-331978
Scientist will now study the role Arp2/3 plays in different parts of the brain, and how its linked to other schizophrenia symptoms. The research is still in its very early stages, and obviously has only been demonstrated in mice and not humans. But it’s a promising first step towards understanding this mysterious disease.
Scott Sodeling: “We’re very excited about using this type of approach, where we can genetically rescue Arp2/3 function in different brain regions and normalise behaviours. We’d like to use that as a basis for mapping out the neural circuitry and defects that also drive these other behaviours.”
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