3 upvotes, 2 direct replies (showing 2)
View submission: Ask Anything Wednesday - Biology, Chemistry, Neuroscience, Medicine, Psychology
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Comment by aTacoParty at 16/03/2023 at 01:08 UTC
2 upvotes, 0 direct replies
First I'd like to say that depression is more than just low monoamine levels in the brain (serotonin and dopamine). While its been popularized that low serotonin levels = sad, depression is a complex and heterogeneous disease that involves other neurotransmitters such as GABA and glycine as well as alterations in brain connectivity. And research into structural and functional brain imaging is a great way to show that.
MRI scans of people with depression have shown a large variety of changes but the most consistent change was decreased size of the hippocampus (memory center). Functionally, we can see decreased overall connectivity between brain regions and particularly decreased connectivity from the prefrontal cortex (executive functions) and other regions.
Unfortunately, the presentation of depression is so varied that its impossible right now to look at a brain scan and tell whether or not someone has depression. Decreased hippocampal volume can be seen in other diseases like Alzheimer's or just aging. Most likely depression (IE major depressive disorder) is actually multiple diseases that have the same presentation. Once we can differentiate these different diseases, we may be able to correlate brain scan changes to disease better than we can now.
MRI for depression: https://www.nature.com/articles/s41398-019-0680-6[1][2]
1: https://www.nature.com/articles/s41398-019-0680-6
2: https://www.nature.com/articles/s41398-019-0680-6
Comment by Brain_Hawk at 16/03/2023 at 03:29 UTC
2 upvotes, 0 direct replies
There are several on average differences that appear to be president people suffering from age depression. One of the great challenges in neuroscience, and particularly a neural imaging, is the issue of individual variability. There are no great predictors of depression. We can't reliably scan a brain to determine if it is or is not depressed, wasn't looking at its structurally or functionally
There are some consistent effects in the brain, but again not sufficient to separate people with depression from those without. But one example of difference is an over connectivity or activation of the default mode network. This is a very high order brain network that is more activated when you are engaged in introspective kind of behaviors or social cognition. A good example of a default heavy state is when you're sitting on the bus staring out the window with your mind. Kind of just wandering
Overactive default mode and depression has been associated with excessive rumination and we're directive thought, including repeated negative thoughts that people can't break out of. There's some evidence that certain treatments for depression, notably deep brain stimulation and repetitive transcription of magnetic stimulation, may work in part by modulating some deep structures in the default mode
But, my key take home is brains are crazy complicated. There's no one size fits all. There's probably a lot of kinds of depression. There's probably a lot of ways for people's brains to become depressed. The one constant is there is no constant. Which is a lot of difference across people's, which makes it hard to map. Really discrete neural circuits for a specific psychiatric problems, though we're doing the best that we can
Certainly visually there's nothing different. As for stuff like serotonin, this is also not a marker of depression. It's not clear at this point. If serotonin is directly related to depression. It's true that serotonergic reuptake inhibitors treat depression, but that doesn't necessarily mean this is causative. Acetaminophen's cause headaches, but headaches aren't caused by a lack of acetaminophen
I feel a bit open-minded about the serotinergic hypothesis of depression right now, I guess we'll see