Researchers prevent schizophrenia progression in mice


Thank god all these working experiments on mice are working, we won’t have to worry about schizophrenic mice running around… now what about humans? When will they actually do experiments that matter to us?


So they gave them APs earlier and it prevented schizophrenia. That’s no help for us though, unfortunately.

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It makes me wonder if I’d been put on an AP at 16 would I be cured now.

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But you would still need to be on APs now though, so would it be that much different?

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First of all, these mice do not have schizophrenia. Second, these studies are some of the first steps in developing new treatments for humans - not for mice. We can’t just do like the nazis and perform dangerous, unethical and involuntary experiments on humans. Whatever your views on morality are, I’m sure they are very far from that alternative.


When will they realize that rats and humans are different and experiments on rat doesn’t mean good results for humans ooo well they r trying

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You really think you know more than these researchers about the difficulties and potential of translating preliminary research on animals into research on humans? Come on. This is what they do for a living. They’ve studied for years to be allowed to do this.


Full PDF


This is very interesting.

Taken together, our results provide evidence that, in adult LgDel+/ mice, PVneurons are present in normal numbers and might not be physiologically abnormal, but their recruitment through excitation is markedly reduced. This is reflected in chronic low-PV plasticity specifically in early-born PV neurons, failure to effectively inhibit PN firing, and failure to induce high-PV plasticity upon chemogenetic activation of PV neurons or learning.

We then carried out D2R antagonist treatments aimed at the vH or dorsal hippocampus (dH) during a P60–P70 time window and monitored possible long-term consequences on PV neuron recruitment and plasticity. Remarkably, single delivery of a D2R antagonist every second day from P60–P70 to the vH (vCA3/CA1) produced long-lasting and brain-wide rescue of PV expression levels in LgDel+/ mice (Figures 4A and S5). Comparable rescue of PV expression values was achieved with haloperidol or with the more specific D2R antagonist eticlopride (Figures 4A and S5). Consistent with long-lasting rescue of PV excitatory recruitment, treated adult mice exhibited no signs of chronic lowPV plasticity, including nearly WT-level PV expression in earlyborn PV neurons and excitatory synaptic punctum densities onto PV neurons (Figures 4B and 4C). Furthermore, inhibitory neuron firing frequencies and activation, PN inhibition, and PV neuron plasticity upon chemogenetic activation of PV neurons were effectively restored in treated adult LgDel+/ mice (Figures 4D and S5). Finally, treated LgDel+/ mice exhibited fear memory and corresponding high-PV plasticity indistinguishable from WT mice upon cFC (Figure S5).

To more clearly define the conditions required to achieve longlasting rescue of PV neuron recruitment in LgDel+/ mice, we carried out a series of additional experiments. In contrast to D2R antagonist treatments aimed at the vH, the same treatment aimed at the dH did not rescue PV expression distributions in adult LgDel+/ mice, either locally or system-wide (Figure S5).

It sounds as though this is very time sensitive:
P60 by the way is post natal day 60, meaning the mice are 60 days old. That corresponds roughly to 20 years in humans, but it’s difficult to make that comparison exactly. I don’t know how many years 10 days of mouse lifespan translates to human years, but probably a couple years at least.

D2R antagonist treatments to the vH from P60–P64 were ineffective, whereas treatments from P60–P66 were as effective as from P60–P70 (Figure S5). Comparable treatments during a P70–P80 time window were much less effective, and 10-day treatments started before P55 or after P75 were ineffective (Figure S5). In further experiments, a D2R antagonist delivered systemically within the P60–P70 time window was as effective as local treatment in the vH, suggesting that similar interventions could be tested in a clinical setting (Figure S5). Taken together, these results define a sensitive time window between P60 and P75 when repeated vH treatments with a D2R antagonist produce long-lasting, system-wide rescue of chronic low-PV plasticity as well as of PV neuron recruitment and plasticity in LgDel+/ mice.

It’s also important to note that these mice were a specific genetic model for SZ, one with adult onset. In people of course there are many different potential genetic causes. Perhaps many of these also relate to the PV interneurons. PV interneuron dysfunction seems to be a core piece of the puzzle - this is also the interneuron type Dr Lodge was studying with the stem cell transplants.

I don’t know, but it’s testable in people if they can figure out how to fairly accurately determine who is at risk for schizophrenia. They’re not going to treat asymptomatic 18, 20, 22 year olds with APs, even every other day, for several years just on the off chance they might later develop schizophrenia. There will have to be an accurate predictive screening tool - which I do think will someday be developed, but it hasn’t been developed yet.


I will say it would probably be quicker if things were done to living human experiments. But the morality of putting human lives in danger interferes with that.

So mice and rats are the starting points for most research that eventually turns into studies on humans, Due to a similar brain structure.

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Right. You cant just inject humans with shít and hope it doesn’t kill them. Using mice is the lesser of two evils.


What in the hell is a schizophrenic mouse?

I think tests would prove a lot more plausible if they take hobos off the street and clone them for science …