Toward Convergence in the Medication Treatment of Bipolar Disorder and Schizophrenia

Citrome, Leslie; Goldberg, Joseph F.; Stahl, Stephen M.

doi:10.1080/10673220590923164

Cited by 24 publications

(17 citation statements)

References 104 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…Common molecular causes have been proposed for affective disorders and schizophrenia (Citrome et al 2005; Craddock et al 2006; Van Den Bogaert et al 2006). Our data suggests bipolar disorder and major depressive disorder are associated with abnormal muscarinic receptor expression, as has been reported in schizophrenia (Dean et al 2003).…”

Section: Discussionmentioning

confidence: 99%

Decreased muscarinic receptor binding in the frontal cortex of bipolar disorder and major depressive disorder subjects

Gibbons

Scarr

McLean

et al. 2009

Journal of Affective Disorders

View full text Add to dashboard Cite

Background-Dysfunction of the cholinergic muscarinic receptors has been implicated in the pathology of bipolar disorder and major depressive disorder. However, there is conflicting evidence regarding the association between individual muscarinic receptors and the two disorders.Methods-We used the muscarinic receptor selective radioligands [ 3 H]pirenzepine, [ 3 H] AFDX-384 and [ 3 H]4-DAMP to measure the levels of muscarinic 1 (CHRM1) and muscarinic 4 (CHRM4) receptors, muscarinic 2 (CHRM2) and muscarinic 4 (CHRM4) receptors and muscarinic 3 (CHRM3) receptor, respectively. Radioligand binding was measured in Brodmann's area (BA) 10 of the rostral prefrontal cortex, BA 46 of the dorsolateral prefrontal cortex and BA 40 of the parietal cortex in the post-mortem CNS from subjects with bipolar disorder or major depressive disorder and control subjects. Limitations-9 bipolar disorder, 9 major depressive disorder and 19 control subjects were used in the study. Publisher's Disclaimer: This is a PDF file of an unedited manuscript that has been accepted for publication. As a service to our customers we are providing this early version of the manuscript. The manuscript will undergo copyediting, typesetting, and review of the resulting proof before it is published in its final citable form. Please note that during the production process errors may be discovered which could affect the content, and all legal disclaimers that apply to the journal pertain. Conclusion-Our data is consistent with previously published data implicating a role for CHRM2 receptors in the pathology of bipolar and major depressive disorder. The demonstration of a novel association between decreased CHRM3 receptor expression and bipolar disorder suggests bipolar and major depressive disorder differ in the underlying nature of their cholinergic dysfunction. Results-[ NIH Public Access

show abstract

Section: Discussionmentioning

confidence: 99%

Decreased muscarinic receptor binding in the frontal cortex of bipolar disorder and major depressive disorder subjects

Gibbons

Scarr

McLean

et al. 2009

Journal of Affective Disorders

View full text Add to dashboard Cite

show abstract

“…Based on the co-administration of second generation antipsychotics with mood stabilizers for BD, mood stabilizers such as lithium or anticonvulsants have been used together with antipsychotics as adjunctive medication for the treatment of schizophrenia, for the same purpose of producing potential synergistic or enhanced responses (Citrome et al, 2005; Johannessen, 2008). Although adjunctive lithium treatment in early studies seemed to be somewhat beneficial (Carman et al, 1981; Kellams et al, 1976; Small et al, 1975), later, well-designed trials found that this treatment strategy did not produce robust evidence of improvement.…”

Section: Lithium In Models Of Cns Disorders and Its Clinical Implimentioning

confidence: 99%

Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders

Chiu

Chuang

2010

Pharmacology & Therapeutics

197

198

View full text Add to dashboard Cite

Lithium has been used clinically to treat bipolar disorder for over half a century, and remains a fundamental pharmacological therapy for patients with this illness. Although lithium’s therapeutic mechanisms are not fully understood, substantial in vitro and in vivo evidence suggests that it has neuroprotective/neurotrophic properties against various insults, and considerable clinical potential for the treatment of several neurodegenerative conditions. Evidence from pharmacological and gene manipulation studies support the notion that glycogen synthase kinase-3 inhibition and induction of brain-derived neurotrophic factor-mediated signaling are lithium’s main mechanisms of action, leading to enhanced cell survival pathways and alteration of a wide variety of downstream effectors. By inhibiting N-methyl-D-aspartate receptor-mediated calcium influx, lithium also contributes to calcium homeostasis and suppresses calcium-dependent activation of pro-apoptotic signaling pathways. In addition, lithium decreases inositol 1,4,5-trisphosphate by inhibiting phosphoinositol phosphatases, a process recently identified as a novel mechanism for inducing autophagy. Through these mechanisms, therapeutic doses of lithium have been demonstrated to defend neuronal cells against diverse forms of death insults and to improve behavioral as well as cognitive deficits in various animal models of neurodegenerative diseases, including stroke, amyotrophic lateral sclerosis, fragile X syndrome, as well as Huntington’s, Alzheimer’s, and Parkinson’s diseases, among others. Several clinical trials are also underway to assess the therapeutic effects of lithium for treating these disorders. This article reviews the most recent findings regarding the potential targets involved in lithium’s neuroprotective effects, and the implication of these findings for the treatment of a variety of diseases.

show abstract

“…Second-generation antipsychotics have emerged as “mood stabilizers”, rivaling classic agents such as lithium and certain anticonvulsants such as valproate and carbamazepine (Citrome et al 2005a). The second-generation antipsychotics, as monotherapies, can successfully treat bipolar mania, even in the absence of psychotic symptoms, as demonstrated by many clinical trials.…”

Section: Is Aripiprazole Worth Using?mentioning

confidence: 99%

A review of aripiprazole in the treatment of patients with schizophrenia or bipolar I disorder

Citrome¹

2006

Neuropsychiatric Disease and Treatment

Self Cite

View full text Add to dashboard Cite

Aripiprazole has been approved by regulatory agencies for the treatment of schizophrenia and bipolar I disorder. Although it is a dopamine partial agonist, it also has substantial binding affinity for the serotonin 5HT2A receptor. Several double-blind randomized clinical trials have established the efficacy and tolerability of aripiprazole within the dose range of 10-30 mg/day for schizophrenia, and 15-30 mg/day for manic or mixed states associated with bipolar I disorder. Relatively few comparative trials with other secondgeneration antipsychotics have been published for schizophrenia, with none available for bipolar disorder. The evidence so far suggests that in terms of efficacy for schizophrenia, aripiprazole is superior to placebo and haloperidol (long term), similar to perphenazine and risperidone, and inferior to olanzapine. Its tolerability profile in patients with schizophrenia appears superior to haloperidol, perphenazine, risperidone, and olanzapine. Efficacy in treating manic or mixed states was established in placebo-controlled trials. Among some patients with bipolar disorder, akathisia and gastrointestinal (GI) complaints can emerge at the start of treatment; however, the GI symptoms were time-limited in many instances. Appropriate dosing may also be important in individualizing therapy to improve tolerability, with lower starting doses becoming more important when adding to, or switching from, another antipsychotic. Aripiprazole appears to have a low propensity for weight gain, a favorable metabolic profile, and no association with hyperprolactinemia.

show abstract

Toward Convergence in the Medication Treatment of Bipolar Disorder and Schizophrenia

Cited by 24 publications

References 104 publications

Decreased muscarinic receptor binding in the frontal cortex of bipolar disorder and major depressive disorder subjects

Decreased muscarinic receptor binding in the frontal cortex of bipolar disorder and major depressive disorder subjects

Molecular actions and therapeutic potential of lithium in preclinical and clinical studies of CNS disorders

A review of aripiprazole in the treatment of patients with schizophrenia or bipolar I disorder

Contact Info

Product

Resources

About