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Mood disorders task 2 Task 2 inflammation :3!! (depression and modern…
Mood disorders task 2
Task 2 inflammation :3!!
Meta analysis
differences in brain activity during emotion processing in mood disorders reported
--> However shown that evidence is not conclusive that there are differences in brain activation
because limitations of metanalysis
also huge study heterogeneity!!
studies for emotion processign all use different designs and ways to measure it
normal studies = not replicated
depression and modern societies
prevelance rising = linked with modern societies as measured by GDP
---> However just a trend and not signif + exceptions like Japan (high modern low depression)
Body to mind connection
if physical problems = can lead to mind problems
true in society
obesity, bad diet, no physical activity, too little sunlight, sleep deprivation, social isolation = all correlate highly with depression
---> shows body/ physical problems correlate highly with mind problems / mood disorders :3!!
obesity = assocaited with neural inflammation
--> so is depression
--> lots of the other ereaders about inflamation so maybe pay attention to that :3 !!
diet
--> mediterranian = less inflammation and depression
#
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physical activity
--> areobic excercise = good treatment against depression
--> jsut as good as antidepressant :D !! (read that study before me thinks :3 !!
sunlight exposure
--> linked with SAD (seasonal affective disorder)
--> depression in shift workers
-->reduced endocrine function / circadic rhythm / vitamin D etc blabla lol
social isolation
--> social network size associated with resiliance to pain etc
--> causes stress = more stress assocaited with depression or something read up again lol
sleep deprivation
nuronal and nurochemichal correlates
--> main point psychological stress can trigger immune response
--> can we create a drug that can influence the immune system to have antidepressant effects
brain areas
NT
monoamine
--> dopa
-->5HT (serotonin)
nonmonoamine
-->
glutamate
-----> (might be associated wit mPFC and ACC (metaanalysis :3))
-->
gaba
----->important for negative feedback loop for HPA axis (but weak evidence as wel
neuroimmune + neuroendocrine
inflammation (white bloodcell count cytokines and microglia)
-->high in depression
--> hgh cytokines = can disrupt 5-HT and dopa production in animal models
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cortisol theory
more cortisol resistant = reduced corticol effectiveness = leads to overactive immune system / increase in cytokines :D!!
Evidence:
impaired cortisol receptors (Gr = gluccorticid receptor)
---> less cortisol sensitivity
= higher cytokines / inflammation responese
lots of GR receptors in hippocampus
hippocampus important for negative feedback HPA axis = more cortisol production cause there is no stop signal
feedback loop interrupted in general cause GR receptors anywhere insensitive
in depression cortical size of hippocampus can be reduced!!
cause cortisol can attack neurons in hippocampus (stress course at uni me thinks it said that)
less GR receptors as well ?
high cortisol can inhibit 5HT and Dopa production
animal studies show this
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cytokine (white bloodcell) theory
immune system responds to psychological stressors as well (cytokine release :3!!)
really they are interrelated
Evidence:
in animal + cell models
can produce neurological changes characteristic for depression
increasing cytokine and reducing cytokine
in small human studies can = induce / reduce depression
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hormones
cortisol