<i>S</i>-Adenosyl Methionine (SAMe) Augmentation of Serotonin Reuptake Inhibitors for Antidepressant Nonresponders With Major Depressive Disorder: A Double-Blind, Randomized Clinical Trial

Papakostas, George I.; Mischoulon, David; Shyu, Irene; Alpert, Jonathan E.; Fava, Maurizio

doi:10.1176/appi.ajp.2009.09081198

Cited by 261 publications

(129 citation statements)

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“…Most studies to date have focused on compounds such as cyclooxygenase (COX) inhibitors or minocycline, (Raison et al, 2013b) COX inhibitors Mixed results in psychiatric patients (Köhler et al, 2014;Sommer et al, 2012) Minocycline Reduced negative symptoms in schizophrenia (Köhler et al, 2014;Sommer et al, 2012) DA synthesis L-DOPA Increased motivation in PD (Czernecki et al, 2002) BH4 Case reports: improves depressive/motor symptoms (Pan et al, 2011;Sato et al, 2014) SAMe Evidence of success as adjuvant in MDD (Papakostas et al, 2010;Sarris et al, 2014;Sarris et al, 2015) L-Methylfolate Evidence of success as adjuvant in MDD (Ginsberg et al, 2011;Godfrey et al, 1990;Papakostas et al, 2012;Shelton et al, 2015) DA receptors D2 agonists Successful adjuvant in unipolar and bipolar depression (Cassano et al, 2004;Cusin et al, 2013;Fawcett et al, 2016;Franco-Chaves et al, 2013) Adenosine A2A antagonists…”

Section: Therapies That Block Inflammationmentioning

confidence: 99%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

280

218

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Motivational and motor deficits are common in patients with depression and other psychiatric disorders, and are related to symptoms of anhedonia and motor retardation. These deficits in motivation and motor function are associated with alterations in corticostriatal neurocircuitry, which may reflect abnormalities in mesolimbic and mesostriatal dopamine (DA). One pathophysiologic pathway that may drive changes in DAergic corticostriatal circuitry is inflammation. Biomarkers of inflammation such as inflammatory cytokines and acute-phase proteins are reliably elevated in a significant proportion of psychiatric patients. A variety of inflammatory stimuli have been found to preferentially target basal ganglia function to lead to impaired motivation and motor activity. Findings have included inflammation-associated reductions in ventral striatal neural responses to reward anticipation, decreased DA and DA metabolites in cerebrospinal fluid, and decreased availability, and release of striatal DA, all of which correlated with symptoms of reduced motivation and/or motor retardation. Importantly, inflammation-associated symptoms are often difficult to treat, and evidence suggests that inflammation may decrease DA synthesis and availability, thus circumventing the efficacy of standard pharmacotherapies. This review will highlight the impact of administration of inflammatory stimuli on the brain in relation to motivation and motor function. Recent data demonstrating similar relationships between increased inflammation and altered DAergic corticostriatal circuitry and behavior in patients with major depressive disorder will also be presented. Finally, we will discuss the mechanisms by which inflammation affects DA neurotransmission and relevance to novel therapeutic strategies to treat reduced motivation and motor symptoms in patients with high inflammation.

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Section: Therapies That Block Inflammationmentioning

confidence: 99%

Inflammation Effects on Motivation and Motor Activity: Role of Dopamine

Felger

Treadway

2016

Neuropsychopharmacol

280

218

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“…Once decarboxylated, SAM is irreversibly committed to the polyamine synthesis pathway. SAM has been recently implicated in MDD as it has been suggested for use as a monotherapy or as an adjunctive treatment for individuals with MDD that do not respond to traditional antidepressant therapies [37]. It is proposed that the antidepressant effect of SAM is mediated by monoamines, as it is a precursor molecule for dopamine, norepinephrine, and serotonin.…”

Section: -Function Of Rate-limiting Enzymes Of Polyamine Biosynthesismentioning

confidence: 99%

Suicide and the Polyamine System

Gross¹,

Turecki

2013

CNSNDDT

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Suicide is a significant worldwide public health problem. Understanding the neurobiology is important as it can help us to better elucidate underlying etiological factors and provide opportunities for intervention. In recent years, many lines of research have suggested that the polyamine system may be dysregulated in suicidal behaviors. Initial research in animals provided evidence of a dysfunctional polyamine stress response system, while later work using post-mortem human brain tissue has suggested that molecular mechanisms may be at play in the suicide brain. In this review, we will describe the research that suggests the presence of alterations in the polyamine system in mental disorders and behavioral phenotypes, with particular attention to work on suicide. In addition, we will also describe potential avenues for future work. KeywordsEpigenetics; Major Depressive Disorder; Neurobiology; Polyamines; Polyamine Stress Response; Spermidine/Spermine-N 1 -Acetyltransferase; Suicide -IntroductionSuicide, most often associated with major depressive disorder (MDD) [1], is an important cause of premature death around the world [2]. According to the World Health Organization (www.who.int, 2012), approximately one million people die by suicide annually, and the rate of suicide attempts is 20 times greater than that of suicide completion (www.who.int, 2012). As such, suicidal behaviors (SB) are an important source of public health concern. The etiology of suicide is complex [3], and commonly understood as resulting from the interaction of predisposing (distal) and precipitant (proximal) factors [4]. Biological alterations resulting from a combination of genetic and environmental risk factors underlie predisposition to suicide, but the exact molecular mechanisms at play remain largely unclear. As such, it is important that we gain a better understanding of the molecular processes associated with suicide in order to identify new avenues for prevention and intervention.Over the past several decades, molecular studies of suicide and MDD have focused on the monoamine system. Beginning in the late 1960s, research into the neurobiology of suicide

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“…Current treatment for depression includes drugs such as selective serotonin reuptake inhibitors, tricyclic antidepressants and monoamine oxidase inhibitors. They are effective and tolerated well but noncompliance due to slow action, low response, and plethora of side effects are generally observed [10][11][12][13][14][15][16][17] . Also they inhibit sexual behavior [18] .…”

Section: (Details On Page 997)mentioning

confidence: 99%