Alpha-1-acid glycoprotein in major depressive and eating disorders

Healy, David; CALVIN, JOSEPH K.; Whitehouse, Andrew M.; White, William J.; Wilton-Cox, Helen; Theodorou, A.; Lawrence, Kevin M.; Horton, Roger W.; Paykel, Eugene S.

doi:10.1016/0165-0327(91)90078-7

Cited by 48 publications

(13 citation statements)

References 18 publications

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“…Evidence suggests that the level of acute phase proteins change during depression. Such studies found an increase in the level of a1-acid glycoprotein [123]. MDD has been correlated with activation of immune system, cellular activation, rise in positive acute phase proteins, and decline of negative acute phase proteins [124] [125] [126].…”

Section: Acute Phase Proteins In Major Depressionmentioning

confidence: 99%

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The Role of Immune System in Depression Disorder

Hoseinzadeh¹,

Abadi²,

Agheltar³

et al. 2016

Health

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In order to diagnose a major depressive disorder, patients must have at least 5 depressive symptoms out of 9 criteria, present for at least two weeks. Depressive symptoms include absence of concentration, fatigue and suicidal ideation. The intensity of depression symptoms affects the severity of depression and the degree of the impact on the quality of life. Major depressive disorders (MDD) are defined as a significant health problem, and are estimated to rise in prevalence in the future years. Immune cytokine, associated with major depression for instance, is the interleukin IL-6 and tumor necrosis factor (TNF-α) which is defined as pro-inflammatory cytokines, can activate an inflammatory response. The effects of other inflammatory cytokines on the central nervous system are of controversy. There is an increasing interest about the effect of cytokines derived from innate immune system on the brain and behavior. Cytokines are defined as large sized proteins, mainly produced by immune cells. Two subtypes of cytokines exist: pro-inflammatory cytokines, facilitating inflammatory responses and neural activities; and anti-inflammatory cytokines, inhibiting inflammatory processes. Besides microglia and astrocytes, immune cells such as monocytes, macrophages, and lymphocytes also produce cytokines. At the times of immunological alterations, infections or inflammation, cytokines will be in an activated form. The main goal of the current review study is to investigate the role of the immune system in the depression disorder.

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Section: Acute Phase Proteins In Major Depressionmentioning

confidence: 99%

“…Other studies have reported an increase in the level of acute phase proteins, C3, C4, immunoglobulin M and cytokines [123] [137] [138] [139].…”

Section: Acute Phase Proteins In Major Depressionmentioning

confidence: 99%

The Role of Immune System in Depression Disorder

Hoseinzadeh¹,

Abadi²,

Agheltar³

et al. 2016

Health

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“…Increased 2 AR density may be consistent with the mechanisms of action of antidepressants which downregulate 2 AR density, particularly in the high-conformational state (Salama et al 1982;Smith et al 1983;Kovachich et al 1993), and may explain the partial efficacy of antidepressants in PTSD (Bleich et al 1986;Falcon et al 1986;Frank et al 1988;Davidson et al 1990Davidson et al , 1993Southwick et al 1997). The notion that upregulation in 2 AR density represents a trait rather than a state marker is further supported by reports of a lack of change in 2 AR density or 2 AR-mediated hormone responses following antidepressant treatment in major depression or panic disorder (Siever et al 1983;Stahl et al 1983;Cooper et al 1985;Healy et al 1991;Butler et al 1992;Kaneko et al 1992;Werstiuk et al 1992;Gurguis et al 1997;Gurguis et al 1998b).…”

Section: Discussionmentioning

confidence: 90%

Platelet α 2 -adrenergic receptor coupling efficiency to G i protein in subjects with post-traumatic stress disorder and normal controls

Gurguis¹,

Andrews²,

Antai-Otong³

et al. 1999

Psychopharmacology

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Low platelet membrane alpha2-adrenergic receptor (alpha2AR) density and low basal and forskolin-stimulated cyclic adenosine monophosphate responses, which have been reported in post-traumatic stress disorder (PTSD), suggest either abnormal alpha2AR coupling to G(i) protein or dysregulation in post-receptor signal transduction mechanisms. alpha2AR density in the high- and low-conformational states, agonist affinity in both states and coupling to G(i) protein were investigated in 23 drug-free combat PTSD patients and 25 normal controls. alpha2AR coupling measures were not different between PTSD patients and controls. Total alpha2AR density was higher in PTSD patients than controls, due to a higher density of the receptor in the high-conformational state. There were no differences in agonist affinity to the receptor in either conformational state. Results rule out dysregulation in alpha2AR coupling to G(i) protein. Studies of post-receptor signal transduction mechanisms are warranted.

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“…Результаты показали, что в группе больных с депрессией показатели агрегации были достоверно ниже, чем в груп-пе здоровых. Авторы предположили существование в сы-воротке депрессивных пациентов фактора, тормозящего агрегацию на уровне активации протеинкиназы С. В каче-стве такого агента рассматривался [39] α 1 -ацид-гликопротеин -острофазовый белок, который ингиби-рует агрегацию, индуцированную АДФ. Это предположе-ние имеет право на существование, поскольку хорошо известна цитокиновая или воспалительная теория депрес-сии и в ряде исследований было показано преобладание провоспалительных цитокинов у больных с депрессивны-ми нарушениями [40].…”

Section: Discussionunclassified