Posted by linkadge on August 13, 2006, at 15:41:00
In reply to Re: Optimistic part » Aphrodite, posted by Dinah on August 13, 2006, at 14:25:44
Its difficult to say that SSRI's are targeting the exact form of neurotrophic deficit seen in depression.
Dr. Manjii, a cellular biologist, who has done a lot of research into mood disorder underpinnins and mood stabilizer action says that the brain abnormalities in depression go beyond atrophy to the hippocampus.
He explains it as mood disorders suffering from neuronal resilliancy deficits. He thinks that those with mood disorders have an imborn disoposition for weak neuronal survival mechanisms.
He is also the one who noticed that while a family history of bipolar or unipolar often correlates with atrophy to the frontal cortex, antidepressants do not treat that atropy. Most anticonvulsant mood stabilisers to not as well. The reason he puts lithium and depakote above other moood stabilizers is in their ability to activate growth factors and neuronal resiliance in many brain regions.Even in his experiements with subtheraputic doses of lithium, he found that there were dramatic increases in BCL-2, and agent that protects brain cells from hypoxia, excess glutamate, free radicals etc. Lithium also increases total grey matter volume and increases stem cell proliferation.
The reason I say that drugs for alzheimers or parkinsons might be usefull for depression is the notion that neurotrophic agents of many different forms are able to reduce depression in animal models. Ampakins, for instance, are agents capable of boosting cognition, learning, and neruogenesis, and are being tested for alzheimers, but show significant overlap with depression.
>forgot to say that the reason I like to think >of depression this way is that this model >renders the atrophy and cell loss as >beingsecondary processes and reversible upon >successful treatment.
Perhaps. It could be too that a regional dysregulation of neuronal survivial mechanisms is the core issue. When a stressfull life event comes around, this deficit imediately translates to a high disposition to depression.
>They are not the primary disease process and >are not necessary to precipitate the illness. I >could be wrong, but this is the way things make >sense to me right now.
I don't know if we know yet how the dysregulation initially occurs. When an antidepressant works, its easy to assume that one is suffering from an antidepressant deficiancy, but it could be from something like a growth factor deficiancy. Research into the association between mood disorders and genes encoding for BDNF production, for instance, are somewhat promising.
As some of the research is showing that a lot of depressed people are developing parkinsons, and a lot of parkinsons patients are developing depression.
Linkadge
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URL: http://www.dr-bob.org/babble/20060810/msgs/676086.html