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Block 8 Week 1 > Inflammation and Depression- Hunter > Flashcards

Inflammation and Depression- Hunter Flashcards

1
Q

Smith suggested that depression was caused by inflammation and acute phase response via cytokines such as (blank, blank, and blank)

A

TNF-alpha, IL-1Beta. and IL-6

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2
Q

Smith also suggested that cytokines gained access to the brain and caused hyperactivity of the (blank), disturbance of (blank) and cause neurovegative symptoms

A

HPA axis

serotonin metablism

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3
Q

What are neurobegative symptoms?

A

sleep disturbances, decreased appetite and energy

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4
Q

App. 1/3rd of people with depression have higher levels of the inflammatory marker (blank)

A

CRP

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5
Q

App. 1/3rd of people with depression have higher levels of the proinflammatory cytokines (blank X 3)

A

TNF-alpha
IL-1B
IL-6

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6
Q

Are the levels of proinflammatoy cytokines and inflammatory maker similiar to levels seen in autoimmune or infectious disease?

A

no

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7
Q

What are the levels of proinflammatoy cytokines and inflammatory markers similiar to?

A

diseases where inflammation in implicated (i.e CV disease, stroke, diabetes)

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8
Q

THe most replicated findings pertain to raised (blank) and (blank). These cytokines may serve as biomarkers for risk or prognostic indicators.

A

CRP

IL-1B

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9
Q

The most replicated findings pertain to raised CRP and IL-1b confirmed by at least two recent meta-analyses. These cytokines may serve as (blank) for risk or (blank)

A

biomarkers

prognostic indicators

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10
Q

T or F

Not all patient with depession have elevated inflammatory mediators

A

T

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11
Q

Why is it difficult to justify depression as an inflammatory illness?

A

because it is neither necessary nor sufficient to be the sole cause of depression

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12
Q

The data supports that inflammation as a feture of depression does exist in a subset of patients and this is due to (Blank) and (Blank) factors for depression

A

environmental

genetic

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13
Q

Is inflammation/immune disruption specific to depression?

A

nope, found in lots of neuropsychiatric conditions including schizophrenia

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14
Q

T or F

depression occurs at a 5-10 times higher rate in those with known inflammatory diseases

A

T

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15
Q

What are the peripheral inflammatory diseases that cause depression?

A

-psoriasis
-rheumatoid arthritis
-IBS
(average rate of depression is 15%)

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16
Q

Depression is also common in diseases of the central nervous system such as (blank)

A

Multiple sclerosis

50% are sad, suicide rate as high a 15%

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17
Q

How do you treat hep c, why is this bad?

A

IFN-alpha and IL-2

->causes a cytokine storm that can resut in depression

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18
Q

(blank) percent of patients treated with IFN-alpha develop clinical depression

A

30

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19
Q

T or F

anti-inflammatory treatments have been associated with antidepressant effects

A

T

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20
Q

What was the “proof” that anti-inflammatories cure depression?

A

gave anti-TNF alpha antibody (infliximab) to Chrohn’s disease patients and it resulted in remission in depression

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21
Q

A study found the (Blank) percent of patients with psoriasis and depression who were treated with (Blank) showed improved becks depression inventory scores , with an effect size comparable to antidepressants. What was awesome about this study?

A

50%

Etanercept (soluble TNF-alpha receptor)

These reults were found to be independent of improvement in psoriasis

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22
Q

A study showed that (blank) added to reboxetine (a selective norepinephrine reuptake inhibitor) improved depressive symptoms more than reboxetine alone.

A

celecoxib

I.e add an anti-inflammatory to an anti-depressant will reduce depression more than an anti-depressant alone

23
Q

What does celecoxib do?

A

Cox 2 inhibitor

24
Q

What were antidepressant shown to reduce levels of (especially SSRI)?

A

IL-1B, IL-6 along with depressive symptoms

note: did not reduce levels of TNF-alpha**

25
Q

Antidepressants block the effect of (blank) in the brain

A

inflammatory cytokines

26
Q

The data suggests that inflammation is associated with depression, however this inflammation induced depression may only occur in a subset of (Blank) susceptible individuals

A

genetically

27
Q

Inflammation may not only act as a (blank) factor that pushes a person into depression, but also as a (blank) factor that may pose an obstacle to recovery

A

precipitating factor

perpetuating factor

28
Q

Inflammatory mediators may be potential (blank), aiding in diagnosis or even helping to predict prognosis

A

biomarkers

29
Q

Treatment with (blank) has promise in some patients with depression

A

anti-inflammatory drugs

30
Q

Can you find cytokines in the brain?

A

yes! they are made their and the brain couldnt survive without them

31
Q

Cytokines in the brain are produced by what ?

A

neurons, microglia, and astrocytes

32
Q

Neurons, microglia and astrocytes have (blank) receptors

A

cytokine

33
Q

Do peripheral cytokine have an effect on the brain?

A

yes through 4 different mechanisms

34
Q

What are the four ways that peripheral cytokines can effect the brain?

A
  • triggering afferents
  • humoral pathway (volume diffusion)
  • humoral pathway 2 (cytokine transporter)
  • secretion of secondary messangers
35
Q

Cytokines produced in the periphery trigger sensory afferents of cranial nerves that transmit signals to the brain. This is called the (blank) pathway. What nerves transmit the signal?

A

(vagal, glossopharyngea nerves)

Neural pathway

36
Q

How do peripheral cytokines get to the brain via the humoral pathway?

A

1) volume diffusion of cytokines from “leaky” circumventricular organs, which lie outside the blood-brain barrier (BBB)
2) saturable cytokine transporters in the BBB

37
Q

How do secondary messangers allow for peripheral cytokines to access the brain?

A

secondary messangers like (PGE2 and NO) are secreted by cells that make up the BBB in response to peripheral cytokines

38
Q

Proinflammatory cytokines can influence the (blank X 3) of autoimmune neurotransmitters like serotonin and dopamine

A

metabolism, production and reuptake

39
Q

Proinflammatory cytokines can have an effect on neuroplasticity by messing with (blank)

A

BDNF

40
Q

Proinflammatory cytokines can affect (Blank) which will influence the production of cortisol thus lessening the inflammatory response and reducing depression. What happens if you dont have this normal response?

A

CRH levels
you will get glucorticoid resistance and lose your feedback mechanism so reduce inflammation and thus will get depression

41
Q

Stress can cause stimulation of the (blank) system which will trigger the release of the neurotransmitter (blank)

A

sympathetic nervous system

NE

42
Q

Macrophages have what kind of receptors and why is this important?

A

adrenergic and ACh reeptors

Cuz when the sympathetic nervous system is triggered by stress, norepinephrine will be released and bind to macrophages.

43
Q

When a macrophage gets bound by NE what happens?

What does this indicate about stress?

A

upregulation of NFkB which increaes proinflammatory cytokines

psychosocial stress can cause depression

44
Q

What can the motor vagus do in regards to inflammation?

A

normally: can downregulate it via ACh

In profound stress: motor vagus system falas apart and wont have negative feedback

45
Q

What is the theory behind glucocorticoid resistance?

A

the inability for your glucocorticoids to inhibit NFkB and thus you get lots of inflammation and then depression

46
Q

Infection or tissue damage recognized by pattern recognition receptors such as (Blank) stimulates (blank).

A

TLR-4

NF-kB

47
Q

Proinflammatory mediators are produced and secreted …what are they?

A

cytokines TNF-alpha, IL-1B, IL-6

48
Q

Cytokines participate in various pathways related to depression. Cytokines can alter (blank) and (Blank) signaling

A

serotonergic and dopaminergic

49
Q

Cytokines participate in various pathways related to depression. Cytokines can activate (Blank) and engage the HPA axis (cortisol production)

A

CRH

50
Q

Cytokines participate in various pathways related to depression. Cytokines can disrupt (blank)

A

synaptic plasticity (BDNF)

51
Q

What do environmental stress do that make you depressed?

A

activate sympathetic neurons that synapse on macrophages via NE and stimulates NF-kB (proinflammatory)

52
Q

Stressors also induce withdrawal of (Blank) input

A

inhibitory motor vagal. I.e wont inhibit NFKB so you have increase in NFkB and increase in proinflammatory cytokines

53
Q

Activation of the mitogen activated protein kinase pathway (MAP- kinase pathway) inhibits the function of (blank), thereby releasing Nf-kB from negative regulation by glucocorticoids (glucocorticoid resistance)

A

glucocorticoid receptors

Block 8 Week 1 (13 decks)

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