Hunter: Inflammation and Depression Flashcards
About 1/3 of people with depression have higher levels of these 4 inflammatory markers in their sera
C-reactive protein
TNF-alpha
IL-1beta
IL-6
**the increased levels are more modest than in autoimmune or infectious diseases, but similar to levels documented in other diseases where inflammation is implicated
The most replicating findings pertain to elevated levels of which two biomarkers or prognostic indicators?
CRP
IL-1beta
What is one argument against inflammation causing depression?
not all patients with depression have elevated inflammatory mediators; inflammation is not necessary or sufficient to be the sole cause of depression
The data support inflammation as a feature of depression in a subset of patients. There is considerable evidence for (blank) and (blank) susceptibility factors for depression
genetic; environmental
Immune/inflammatory disruption has been found in a number of other neuropsychiatric conditions, including (blank), so it’s not specific for depression
schizophrenia
Depression occurs at a (blank) times higher rate in those with known inflammatory diseases
5-10x
The association between inflammation and depression has been seen in the following conditions…
psoriasis
rheumatoid arthritis
inflammatory bowel disease
Depression is also common in diseases of the central nervous system (CNS) such as (blank), with a lifetime prevalence of around 50% and rates of suicide as high as 15%
MS
T/F: Even cancer, stroke, coronary artery disease, and epilepsy that are not traditionally considered to have a primary inflammatory etiopathology, are risk factors for depression
True
Patients who receive cytokines such as IFNalpha and IL-2 as immunotherapy for the treatment of hep C and cancer are more prone to develop (blank)
depression
The prevalence of IFN-alpha induced depression in those treated for hep C?
30%
30% of patients treated with (blank) develop clinical depression
IFN-alpha
Patients with Crohn’s disease and concomitant depression had significant remission from depression after treatment with infliximab, a (blank) antibody
anti-TNFalpha
T/F: 55% of patients with psoriasis and depression who were treated with etanercept (TNF-a receptor blocker) showed improved Beck’s depression inventory scores
True
Which had greater effects on improving depression?
reboxetine alone (NE reuptake inhibitor)
OR
in combination with celecoxib (COX-2 inhibitor which inhibits PGE2)?
the combination of reboxetine with celecoxib improved depression symptoms more than reboxetine alone
A meta-analysis of 22 antidepressant treatment studies found that IL-1b and IL-6 levels (but not TNF-a) (blank) in response to SSRI therapy, along with a reduction in depressive symptoms. These findings propose the possibility that inflammatory cytokines contribute to depressive symptoms, and that antidepressants block the effect of (blank) on the brain
decreased; inflammatory cytokines
**this suggests that these meds have some role in reducing cytokines –> further suggests that cytokines do play a role in depression
It seems that inflammation may play a role in depression only in a subset of (blank) individuals
genetically susceptible
Inflammation is not only a precipitating factor that pushes a person into depression, but also a (blank) factor that may pose an obstacle to recovery
perpetuating
T/F: Treatment with anti-inflammatory drugs has promise in some patients with depression
True
Inflammatory mediators may be potential (blank), aiding diagnosis or even helping to predict prognosis
biomarkers
Cytokines are produces by these three structures…
neurons
microglia
astrocytes
Neurons, microglia and astrocytes produce cytokines and have cytokine (blank)
receptors
4 mechanisms by which peripheral cytokines access the brain?
- cytokines produced in the periphery trigger sensory afferents of cranial nerves which transmit signals to the brain
- humoral pathway which involves volume diffusion of cytokines from leaky organs outside of the BBB
- another humoral pathway that involves saturable cytokine transporters in the BBB
- secretion of secondary messengers (PGE2 and NO) by various cells that constitute the BBB in response to peripheral cytokines
A. Infection or tissue damage recognized by pattern recognition receptors (e.g. TLR-4) stimulates (blank)
B. Proinflammatory mediators are produced and secreted (e.g.: what three cytokines?)
C. Cytokines gain access to the brain, or signal the brain to make (blank)
D. Cytokines participate in various pathways related to (blank)
NF-kB;
IL-6, TNFalpha, IL1beta;
cytokines;
depression
