Antidepressive treatment as a modulator of inflammatory process in patients with heart failure: Effects on proinflammatory cytokines and acute phase protein levels

Tousoulis, Dimitris; Drolias, Apostolos; Antoniades, Charalambos; Vasiliadou, Carmen; Marinou, Kyriakoula; Latsios, George; Stefanadi, Elli; Gounari, Panagiota; Siasos, Gerasimos; Papageorgiou, Nikolaos S.; Trikas, Athanasios; Stefanadis, Christodoulos

doi:10.1016/j.ijcard.2008.02.013

Cited by 38 publications

(38 citation statements)

References 24 publications

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“…However positive data exists also in favor of TCAs/serotonin norepinephrine reuptake inhibitors (SNRIs). In a recent study we conducted in HF patients [8], circulating levels of proinflammatory molecules were decreased in those HF patients under TCA/SNRI treatment compared to those under SSRIs or without Fig. 1.…”

Section: • Underlying Biological Mechanismsmentioning

confidence: 85%

“…depression. TCA/SNRIs significantly reduced plasma levels of proinflammatory cytokines, like ΙL-6 and TNF-a, as also of acute phase reactants like CRP and fibrinogen, all molecules with a predictive value in HF [8].…”

Section: • Underlying Biological Mechanismsmentioning

confidence: 94%

“…HF patients with major depression are at increased cardiovascular mortality risk compared to non-depressed patients [6]. Furthermore, evidence suggests that antidepressants have various cardiovascular side effects and may also negatively affect clinical outcome of HF [7,8].…”

Section: Introductionmentioning

confidence: 99%

See 2 more Smart Citations

Role of depression in heart failure — Choosing the right antidepressive treatment

Tousoulis¹,

Antonopoulos²,

Antoniades³

et al. 2010

International Journal of Cardiology

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Section: • Underlying Biological Mechanismsmentioning

confidence: 85%

Section: • Underlying Biological Mechanismsmentioning

confidence: 94%

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Role of depression in heart failure — Choosing the right antidepressive treatment

Tousoulis¹,

Antonopoulos²,

Antoniades³

et al. 2010

International Journal of Cardiology

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“…However, no significant effect of imipramine was found in hippocampus. It is well known that imipramine (Dredge et al, 1999) and its main metabolite, desipramine (Huang et al, 2007), like tricyclic antidepressants (Tousoulis et al, 2009), induced an inhibition in TNF-␣ expression, but the detailed molecular mechanisms underlying these anti-inflammatory effects in the CNS are unknown. Our hypothesis was that imipramine, by modulating TNF-␣ in the CNS could lead to neuroprotection in AD.…”

Section: Discussionmentioning

confidence: 99%

Imipramine, in Part through Tumor Necrosis Factor α Inhibition, Prevents Cognitive Decline and β-Amyloid Accumulation in a Mouse Model of Alzheimer's Disease

Chavant¹,

Deguil²,

Pain³

et al. 2009

J Pharmacol Exp Ther

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Alzheimer's disease (AD), the most common form of dementia in the older people, is a multifactoral pathology, characterized by cognitive deficits, increase in cerebral deposition of the ␤-amyloid (A␤) peptide, neurofibrillary tangles, and neurodegeneration. Studies currently support a central role of neuroinflammation, through production of proinflammatory cytokines including excess tumor necrosis factor ␣ (TNF-␣) in the pathogenesis of AD, especially in A␤-induced cognitive deficits. Imipramine, a tricyclic antidepressant, has potent anti-inflammatory and neuroprotective effects. This study investigates the effect of imipramine on alterations of long-term and short-term memories, TNF-␣ expression, and amyloid precursor protein (APP) processing induced by intracerebroventricular injection of A␤25-35 in mice. Mice were treated with imipramine (10 mg/kg i.p. once a day for 13 days) from the day after the A␤25-35 injection. Memory function was evaluated in the water-maze (days 10 -14) and Y-maze (day 9) tests. TNF-␣ levels and APP processing were examined in the frontal cortex and the hippocampus (day 14). Imipramine significantly prevented memory deficits caused by A␤25-35 in the water-maze and Y-maze tests, and inhibited the TNF-␣ increase in the frontal cortex. Moreover, imipramine decreased the elevated levels of A␤ both in frontal cortex and hippocampus with different modulations of APP and C-terminal fragments of APP. So, imipramine prevents memory impairment through its intrinsic property to inhibit TNF-␣ and A␤ accumulation and may represent a potential candidate for AD treatment.Alzheimer's disease (AD), the most common form of dementia in older people is associated with cognitive deficits. Indeed, brains of individuals who have AD manifest massive neuronal and synaptic loss in certain areas that result in memory impairment and disorientation associated mainly with late stages of the disease. However, in the early stages, the etiology of these cognitive dysfunctions is unclear. AD is a multifactoral pathology, characterized not only by an increase in cerebral deposition of the ␤-amyloid (A␤) peptide, the major constituent of senile plaques that can potentially cause cognitive impairments, but also by neuroinflammation, oxidative damage, and neurodegeneration in critical brain regions (hippocampus, frontal cortex) also involved in memory and cognition

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“…Twin studies found common genetic control of depressive symptoms and inflammatory markers [81]. Pharmacological antidepressive treatment with selective serotonin-reuptake inhibitors or tricyclic antidepressants was found to lower levels of TNF-α and CRP [82].…”

Section: Psychosocial Factorsmentioning

confidence: 97%

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

Kolb¹,

2009

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The recent major increase in the global incidence of type 2 diabetes suggests that most cases of this disease are caused by changes in environment and lifestyle. All major risk factors for type 2 diabetes (overnutrition, low dietary fibre, sedentary lifestyle, sleep deprivation and depression) have been found to induce local or systemic low-grade inflammation that is usually transient or milder in individuals not at risk for type 2 diabetes. By contrast, inflammatory responses to lifestyle factors are more pronounced and prolonged in individuals at risk of type 2 diabetes and appear to occur also in the pancreatic islets. Chronic low-grade inflammation will eventually lead to overt diabetes if counter-regulatory circuits to inflammation and metabolic stress are compromised because of a genetic and/or epigenetic predisposition. Hence, it is not the lifestyle change per se but a deficient counter-regulatory response in predisposed individuals which is crucial to disease pathogenesis. Novel approaches of intervention may target these deficient defence mechanisms.

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Antidepressive treatment as a modulator of inflammatory process in patients with heart failure: Effects on proinflammatory cytokines and acute phase protein levels

Cited by 38 publications

References 24 publications

Role of depression in heart failure — Choosing the right antidepressive treatment

Role of depression in heart failure — Choosing the right antidepressive treatment

Imipramine, in Part through Tumor Necrosis Factor α Inhibition, Prevents Cognitive Decline and β-Amyloid Accumulation in a Mouse Model of Alzheimer's Disease

The global diabetes epidemic as a consequence of lifestyle-induced low-grade inflammation

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