yes dear, we r working on depression, psychosis and other neurological disorders in our lab.

Were you thinking that an auditory exam, might indicate psychiatric symptomology?

We have found that chronic stress produces atrophy of inferior colliculus and impairs auditory avoidance conditioning, in rats. It's also known that stress and deafness are risk factors to depression in old people, but I think stress can alter the function of auditory system, even lead to deafness. It could play some rol in the psichopatholgy of schizophrenia also.

Currently in our lab we are working no more with rats, but I can still run Auditive Evoked Potential tests on patients. I don't know this is worth researching.

If you can get funding, it might be a possible non-destructive confirmation of the stress/depression Axis. Especially if there is a noticeable difference in say the frequency of the decay than that found in damage caused by loud noises, etc. Right now, depression is seen as a soft diagnosis because it is a subjective evaluation of the owner individuals state. By finding external indicators, doctors could send a patient directly to a hearing test, and if the protocol was easily understood, evaluate the results for the "Depression Pattern" confirming the patients condition. As a long-term depressive however, I would suspect that early intervention by this technique would be difficult, since you don't become deaf overnight.

We also have found that the atrophy of inferior colliculus can be prevented with the use of fluoxetine, or even functional food with hight content of omega-3 PUFA.

I think the first step would be compare pattients to controls, and see if it's a external indicators as you say. Then after SSRI treatment, look for a improvement in depressive symptoms and auditory tests.

I need to learn more about auditory evoked potential for know

thank you all for your feedback, any comment is wellcome

We also have found that the atrophy of inferior colliculus can be prevented with the use of fluoxetine, or even functional food with hight content of omega-3 PUFA.

I think the first step would be compare pattients to controls, and see if it's a external indicators as you say. Then after SSRI treatment, look for a improvement in depressive symptoms and auditory tests.

I need to learn more about auditory evoked potential for know

thank you all for your feedback, any comment is wellcome

Right, but how do you deal with the people that respond differently to fluoxetine and omega-3 PUFA

I suspect that there is a small number of us, that do not respond at the usual dosage, or who's symptoms increase despite fluoxetine. I myself have gone through about 15 drugs during my tenure, and each one has responded early and then failed to end my depression, until respiridal.

Is their failure an indication that the inferior collicus is NOT always associated with depression, or is it an indication that some people continue to degrade despite collicus treatment with fluoxetine?

there is so much information about depression, but understand it is the big deal. Many patiens don't responde to fluoxetine, about 30% at first attemp, or less. It's because the serotonine is not the final solution, as it was though decades ago. The man who cure depression with one treatment will earn the Nobel prize. For my self I want to understand the implications of this nucleus of the mid brain in the neurobiolgy of depression, and if it is relevant at a clinical level. why this nucleus is so affected? maybe it's not just an auditory nucleus.

In our rat models, chronic stress affects inferior colliculus, as well structures known to be related with depression as hippocampus, prefrontal cortex, amygdala. As they are rat we can not say that they are suffering depression, but it works as a model of study. so you re correct we cannot say that the dendritic athrophy of IC is always associated to depresion. Maybe it doesn't happens in humans.

Interestly, in humans with schizzophrenia, they have de right IC of lower size than controls.

Have you considered the glial model of Stress reducing dendritic mass in neurons?

In this model, Stress and Inflamation cause glial helper cells to detach from the neurons and migrate to the stress/Inflamation site. In occasional stress situations, the local stem cells can replace them so that the neurons remain supported by glial function, but in chronic stress the stem cells cannot replace the glial cells as they migrate, and so the net effect is a loss of support for the neurons. Since Glial function is strongly indicated in steering dendrites this may be reflected in a loss of direction for dendritic growth resulting in a loss of function of new dendrite growth, which in turn, results in pruning of non-functional dendrites and a net reduction of dendrites that have relevance to the signals passing through the organ involved.

If as Alkon suggests PKC acts as feedback between the firing of the neuron and its synaptic sequestering of proteins, which may be linked to long term memory management ala Kandellian DNA based dendritic growth, fewer dendritic feedback matches will result in less dendritic growth, so we get a reducing system that may in the end result in schizophrenia.

The Inferior Collicus could be especially vulnerable to this degradation possibly because of its involvement in the stress/inflamation systems, or because of a particularly small population of stem cells per glial cell, or some other unknown factor.

The fact that only 30 percent respond to fluoxetine suggests that in fact, there might be three different factors all affecting the inferior collicus. Perhaps the third one is pain.

A rather surprising result was found by a researcher that injected a morphine based chemical into the pancrease of diabetic mice. He claimed complete remission of the diabetes. Diabetes is comorbid with depression, and so one could suppose albeit the evidence is not there yet, that chronic pain could also eventually destroy the inferior collicus. Chronic pain researchers have noted a similar migration pattern for glia during chronic pain. Perhaps the same mechanism is involved in all three cases, but because the source of the problem lies in a different areas, the other sources of depression are not treated by serotonin re-uptake.

If the tendency for the pancrease to get worse over the life of a diabetic, is any indication perhaps other organs are also suffering from glial separation, and the Inferior collicus is merely the most obvious degradation because for some reason it acts as a focal point for the process. The recovery of the pancreas might indicate that all we really need is to give the stem cells a chance to rebuild the glial population and eventually the system will recover.

Well, anyway, enough speculation, if the glial model is correct, you might find that your auditory test gives evidence for not only depression but chronic conditions such as chronic inflamation, chronic stress and chronic pain, and that therefore, they represent opportunities for treatment regimens that treat each in turn until a solution is found. Having a test that confirms chronic pain would also be valuable in that much of the current recovery system is based on the idea that patients are over-reporting due to an addiction to pain medicine instead of the alternate which is that they are over-reporting due to a lack of pain medication where it is necessary.

you give me many valuable information and ideas I really apreciate it Mr Smith

I hope it makes it easy to finance your research. Good luck!

On a different track, someone who watched a popular doctor television show asked me about a link between Alzheimer's disease and diabetes. Apparently there is research to show that AD develops when the brain becomes insulin resistant. Is anyone aware of such research? Could you steer me to documentation?

It is relatively new research, I just saw a website the other day, through BBC's World Service that mentioned it.... Essentially it seems to affect the ability of the brain to communicate, and that snowballs into dementia by adding to the plaques in the blood vessels. No I can't remember enough detail to be useful, attribution is hell for me, but yes, there has been a recent publishing of such a study. As per usual, cautious interest has been expressed by the diabetic research groups.

Ok I googled it. back in 2008 an article was published.

www.science daily.com/releases/2008/04/080430125254.htm

It was corroborated in 2009, by the mayo clinic

The current popularity probably comes from the BusinessWeek article that explains how Insulin Resistance is related to plaque formation. Sorry I couldn't give you the actual address but Google has shortened the URL.

I searched google with Diabetes link to Alzheimers.

I hope that helps.

Ron you can keep that thread over here http://www.researchgate.net/group/Neuroscience/board/thread/26531_Insuline_and_Alzheimer_Disease

thank you

Thank you Graeme. I was able to find a 2010 article on Medscape that answered my questions.