maybe the gut, maybe the genes, don’t know.
It’s something new every day I think
I tried a probiotic supplement and it drove me nuts.
guess work and theories. I don’t think they’ll ever know in my lifetime. Meanwhile I guess I’ll be my evil pdocs lab monkey.
Oh what’s next 
I think @firemonkey posted something recently about them detecting rapid changes in gene expression among schizophrenics…
Neatly cutting edge type thing to attempted to correlate. Shows why we lack a real refineable stability aside from just gaining more experience with the illness.
It’s just a feeling… but based on how indirect everything else seems to influence mental conditions… something like gene-expression shifts… in abnormal amounts due to stress… seems more likely to produce the illusive nature and inconsistency between a brain before psychotic break and then afterward.
Read the article… and they are talking more about the blood brain barrier than the vessels.
Good research to see. It looks like that’s their devout approach so that’s cool to see more fully explore.
Interesting. Probably nothing but my brain blood vessels are probably smaller than normal due to excessive caffeine.
Dont forget the cigs too!
Jealousy…………………….
Okay, a solution:
Gather a team of specialists who have their own idea of how schizophrenia is developed.
Make a report with a collection of different claims.
Neuron-Glia Interactions in Development and Disease
It is becoming increasingly clear that glial cells play a crucial and dynamic role at the synapse during the critical period when neural circuits are formed and refined. The Stevens lab seeks to understand how neuron-glia communication facilitates the formation, elimination and plasticity of synapses—the points of communication between neurons—during both healthy development and disease.
A major goal of our lab is to elucidate the cellular and molecular mechanisms underlying activity-dependent synapse elimination during health and disease, with emphasis on the role of microglia and immune molecules in this process. Using the visual system as our primary model system, we employ a combination of live imaging, molecular, biochemical and neuroanatomical approaches.
In one line of investigation, we focuse on the role of neuron-glia-immune signaling in the patterning of neural circuits. We recently identified an unexpected role of glia and components of the innate immune system in synaptic pruning. We found that astrocytes promote neuronal expression of complement C1q, the initiating protein of the classical complement cascade. C1q binds to synapses and is required for synapse elimination in the developing visual system. As one of the primary roles of complement in the immune system is to mark unwanted cells or debris for removal, we hypothesize that C1q may be similarly “tagging” unwanted synapses for elimination in the brain. Importantly, we found that C1q becomes aberrantly upregulated and is relocalized to synapses at early stages of glaucoma and other neurodegenerative diseases suggesting a similar elimination mechanism may be in place.
Our current studies are aimed to define cellular and molecular mechanisms underlying complement dependent and independent synapse elimination during development and disease. Current research questions include: How are CNS synapses selectively targeted for elimination? Is complement-dependent synapse elimination an activity-dependent process? What is the role of astrocytes and microglia in synapse development and elimination?
Contact
Boston Children’s Hospital
F.M. Kirby Neurobiology Center
Center For Life Science, Room 12-257
3 Blackfan Circle
Boston, MA 02115
beth.stevens@childrens.harvard.edu
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Website
Research Areas
Cellular & Molecular
Developmental
Sensory & Motor Systems
Affiliations
Harvard Medical School
Boston Children’s Hospital
Harvard Brain Science Initiative
Office of the Provost, Smith Campus Center
Harvard University, Cambridge MA 02138
Email: info@brain.harvard.edu
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I like how you got this from RTE. that’s our local broadcaster
As I understand this, what this means is that schizophrenia is caused by when the pruning process starts like a pac man some healthy synapses are eaten up and hence schizophrenia. The pruning process is what all brains do but in the case of a brain that the genes have expressed wrongly this pruning process gets out of control and too many brain cells or neurons are destroyed.But there are so many neurons that this can be over come by the fact that our brains have plasticity.
I didn’t get this from RTE. I got it from a Harvard newsletter. I’m inclined to believe that it’s not vascular by a malfunction of the pruning process as stated in the post I put up!
I think it’s safe to say it can be, and perhaps even probably is, caused by many different things.
That would offer an explanation for why a single cause has been impossible to find, but many risk factors have been identified. It would also explain why some treatments work great for some people and don’t work at all, or partially work for others. If you fix part of the problem you get partially better, KWIM?
This could be part of the puzzle. I believe they’re saying the same about Alzheimer’s too.
Do any of you keep track of the vast number of supposed possible causes of schizophrenia ?
I have lost count.
If schizophrenia was just about biological factors, psychiatrists wouldn’t recommend us to go to psychologist.