New Cause of Schizophrenia Uncovered
According to an article featured on Neuroscience News, studies are indicating that glial cells may just be the
unsung heroes of the nervous system after all. Scientists have discovered a possible
genetic link involved in the development of schizophrenia and other irregular brain
functions that involves the production of glial cells or lack thereof. These genetic defects may cause a depletion
of glial cells resulting in less myelin, the fatty layer that surrounds the
axon of a neuron. The brain develops according to a set of instructions that is
determined by progenitor cells. These progenitor cells then transform into
glial cells. Glial cells are essential to facilitating the synaptic networks
and the transfer of information throughout different parts of the brain. Genes
that damage these progenitor cells end up delaying the maturation of glial
cells, resulting in fewer healthy glial cells overall. Scientists took
progenitor cells from schizophrenic patients and injected them into the brains
of mice. This experiment showed that ineffective glial cells led to abnormal
brain development. The mice had less fatty tissue (myelin sheath) and
astrocytes. These brain conditions led to many negative behaviors implicated in
schizophrenia including poor motor coordination, anxiety, and disordered sleep
patterns. Further research is attempting to replace the defective glial cells
with fully functioning ones in order to alter the prognosis of the disease.
This relates back to numerous areas within psychology. In class, glial cells were
emphasized as part of healthy brain function. They perform numerous necessary
processes like responding to injury & disease and providing scaffoldings
for migrating neurons. Our brains begin to deteriorate without them, resulting
in a plethora of adverse effects like Multiple Sclerosis and apparently
Schizophrenia. In Abnormal Psychology, I learned that schizophrenia is a highly
heritable disease. This study further emphasizes how certain inherited genes
play a role in the development of schizophrenia. Also in one of my other
classes, Ethology and Comparative Psychology, I learned (briefly) about Epigenetics
and the role the environment plays in certain gene expression without altering
the DNA. An example given was of rats exposed to more maternal contact resulted
in less fear due to an increase in expression in the glucocorticoid gene. It is
a constant interaction between our genes and environment that produce the
behaviors we are able to observe in both human and non-human animals. It would
be quite interesting to see how the above article and schizophrenia in general relates
to an epigenetic framework.
This article is making me think about the classification debates about schizophrenia. There's debate about whether it should be classified as a neurodevelopmental disorder or a neurodegenerative disorder. I am interested in how this development about glial cells will contribute to the classification of the disorder. I'm also curious as to how this may change the diagnosis of schizophrenia, as this is a disorder that is usually defined by its symptoms and not by any particular biological basis.
ReplyDeleteThis article fascinated me greatly as, also through Abnormal, I knew that Schizophrenia was a highly genetically related disorder, but I had never thought of it being capable of transcending species. It had never occurred to me that the same dysfunctions that it causes in humans could also be seen in other animals. As it is one of the still most puzzling disorders we know of, this is a greatly interesting point. I wonder that in the opposite of this experiment, if there would be a way to extract of all of faulty glial cells, or add the missing ones, and provide a cure, or at least treatment for the disorder. This disorder and article just heighten the awareness of the importance of sufficient myelination around cells to function properly.
ReplyDeleteAs causes of schizophrenia gain interest, researchers are also particularly curious on why this mental disorder is so difficult to treat. The reason manifests within the biochemistry of schizophrenia. First off, dopamine is the neurotransmitter involved. Dopamine is very difficult to control. Schizophrenics have excess dopamine receptor activation, and so tranquilizers are used to reduce levels, but their levels often fall below the preferred range, causing tardive dyskinesia. In addition, the deficit of dopamine will create Parkinson-like symptoms called tardive dyskonesia. Once these symptoms ramp up, an individual will have to begin taking additional medication. Overtime, the abundance of numerous medications may cause some schizophrenics to have zero response to any type of medication prescribed. Some researchers believe this is due to permanent brain damage within the schizophrenic.
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