Effect of antidepressants on brain-derived neurotrophic factor (BDNF) release from platelets in the rats

Watanabe, Kimihiko; Hashimoto, Eri; Ukai, Wataru; Ishii, Takao; Yoshinaga, Toshihiro; Ono, Takafumi; Tateno, Masaru; Watanabe, I.; Shirasaka, Tomohiro; Saitô, Satoshi; Saito, Toshikazu

doi:10.1016/j.pnpbp.2010.07.036

Cited by 47 publications

(39 citation statements)

References 24 publications

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“…There is also evidence that genetic factors related to patient susceptibility to MDD may correlate with treatment response85 and potentially improve prevention, diagnosis, and treatment. New therapeutic targets include brain regions regulating circadian rhythms, the immune system,86–88 and neurotrophins 89–91. In addition, N -methyl-d-aspartate antagonists to target stress-related perturbation of the hypothalamic pituitary axis are currently being explored 92–95.…”

Section: Resultsmentioning

confidence: 99%

A Review of Antidepressant Therapy in Primary Care

Kennedy¹

2013

Prim. Care Companion CNS Disord.

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Objective: To provide general practitioners with a comparison of major depressive disorder treatments received in primary care and psychiatric clinic settings, a focus on treatment outcomes related to currently prescribed antidepressants, and a review of new and emerging therapeutic strategies.Data Sources: English-language evidence-based guidelines and peer-reviewed literature published between January 1, 2005, and December 31, 2011, were identified using PubMed, MEDLINE, and EMBASE. All searches contained the terms major depressive disorder and unipolar depression, and excluded the terms bipolar disorder/manic depressive disorder. The following search terms were also included: naturalistic study, antidepressant, relapse, recurrence, residual symptoms, response, remission, sequential medication trials, and treatment-resistant depression.Study Selection: Meta-analyses, systematic reviews, and practice guidelines were included. Bibliographies were used to identify additional articles of interest.Data Extraction: Abstracts and articles were screened for relevance to primary care practice. Population-based studies and those involving patients treated in primary care were used whenever possible.Data Synthesis: Achieving remission from a major depressive episode is important to improve functional outcomes and to reduce relapse and recurrence. Despite the availability of numerous antidepressants, as many as 50% of patients require treatment modifications beyond first-line therapy. Among remitters, 90% report residual symptoms that may interfere with function. Patients treated in primary care often have chronic depression (symptom duration ≥ 24 months at presentation) and medical comorbidities. These are clinical predictors of worse outcomes and require individualized attention when treatment is initiated. Antidepressants differ in efficacy, tolerability, and side effects—factors that may affect adherence to treatment.Conclusions: Major depressive disorder is highly prevalent in primary care and is among the most common causes of loss of disability-adjusted life-years worldwide. There are few differences in clinical profiles between depressed patients in primary care and those in specialist clinics, although differences in symptoms and comorbid conditions among individual depressed patients present a challenge for the physician providing individualized treatment. The goal of treatment is remission with good functional and psychosocial outcomes. Physicians in primary care should have expertise in working with a number of current antidepressant approaches and an awareness of new and emerging treatments.

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Section: Resultsmentioning

confidence: 99%

A Review of Antidepressant Therapy in Primary Care

Kennedy¹

2013

Prim. Care Companion CNS Disord.

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“…It is therefore possible that a general decrease in platelet levels occurred following treatment with the combination of doxorubicin and cyclophosphamide. Furthermore, it was reported that antidepressants increase the level of circulating BDNF by stimulating BDNF release from platelets [40]. BDNF can cross the blood-brain barrier via a high-capacity saturable transport system [41] and a correlation between serum BDNF and brain BDNF has been documented [42].…”

Section: Discussionmentioning

confidence: 99%

Doxorubicin and cyclophosphamide treatment produces anxiety-like behavior and spatial cognition impairment in rats: Possible involvement of hippocampal neurogenesis via brain-derived neurotrophic factor and cyclin D1 regulation

Kitamura

Hattori

Yoneda

et al. 2015

Behavioural Brain Research

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“…The rat arcadlin gene is homologous to human protocadherin 8 ( PCDH8 ), in which polymorphisms have been associated with susceptibility to schizophrenia (Bray et al, 2002), as is also the case for cpg15 (Chandler et al, 2010). Genetic studies have linked bdnf to depression (reviewed in Watanabe et al, 2010). Additionally, several other human cognitive disorders have been linked to mutations in genes involved in regulating activity-dependent transcription.…”

Section: Discussionmentioning

confidence: 99%

Activity-regulated genes as mediators of neural circuit plasticity

Leslie

Nedivi

2011

Progress in Neurobiology

108

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Modifications of neuronal circuits allow the brain to adapt and change with experience. This plasticity manifests during development and throughout life, and can be remarkably long lasting. Many electrophysiological and molecular mechanisms are common to the seemingly diverse types of activity-dependent functional adaptation that take place during developmental critical periods, learning and memory, and alterations to sensory map representations in the adult. Experience-dependent plasticity is triggered when neuronal excitation activates cellular signaling pathways from the synapse to the nucleus that initiate new programs of gene expression. The protein products of activity-regulated genes then work via a diverse array of cellular mechanisms to modify neuronal functional properties. They fine-tune brain circuits by strengthening or weakening synaptic connections or by altering synapse numbers. Their effects are further modulated by posttranscriptional regulatory mechanisms, often also dependent on activity, that control activity-regulated gene transcript and protein function. Thus, the cellular response to neuronal activity integrates multiple tightly coordinated mechanisms to precisely orchestrate long-lasting, functional and structural changes in brain circuits.

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Effect of antidepressants on brain-derived neurotrophic factor (BDNF) release from platelets in the rats

Cited by 47 publications

References 24 publications

A Review of Antidepressant Therapy in Primary Care

A Review of Antidepressant Therapy in Primary Care

Doxorubicin and cyclophosphamide treatment produces anxiety-like behavior and spatial cognition impairment in rats: Possible involvement of hippocampal neurogenesis via brain-derived neurotrophic factor and cyclin D1 regulation

Activity-regulated genes as mediators of neural circuit plasticity

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