A shared framework for the common mental disorders and Non-Communicable Disease: key considerations for disease prevention and control

O’Neil, Adrienne; Jacka, Felice N.; Quirk, Shae E.; Cocker, Fiona; Taylor, C. Barr; Oldenburg, Brian; Berk, Michael

doi:10.1186/s12888-015-0394-0

Cited by 103 publications

(79 citation statements)

References 34 publications

(39 reference statements)

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“…These include greater thinning of the grey matter, which is most pronounced within the pre-frontal cortex, as well as greater disrupted thalamo-cortical functional connectivity at baseline (Cannon, 2015), which may provide potential prognostic clues as to the risk of future progression within high risk populations. In order for any of the above early therapeutic interventions to be effective however, preventative paradigms need to be integrated within mental health in partnership with other medical disciplines and health promotion agencies (O’Neil et al, 2015). A greater understanding of the potential hits and vulnerability factors which work together to drive the pathophysiology of schizophrenia will be required in order to make such preventative programs feasible.…”

Section: Prevention Strategiesmentioning

confidence: 99%

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

Davis

Eyre

Jacka

et al. 2016

Neuroscience & Biobehavioral Reviews

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279

209

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Schizophrenia risk has often been conceptualized using a model which requires two hits in order to generate the clinical phenotype—the first as an early priming in a genetically predisposed individual and the second a likely environmental insult. The aim of this paper was to review the literature and reformulate this binary risk-vulnerability model. We sourced the data for this narrative review from the electronic database PUBMED. Our search terms were not limited by language or date of publication. The development of schizophrenia may be driven by genetic vulnerability interacting with multiple vulnerability factors including lowered prenatal vitamin D exposure, viral infections, smoking intelligence quotient, social cognition cannabis use, social defeat, nutrition and childhood trauma. It is likely that these genetic risks, environmental risks and vulnerability factors are cumulative and interactive with each other and with critical periods of neurodevelopmental vulnerability. The development of schizophrenia is likely to be more complex and nuanced than the binary two hit model originally proposed nearly thirty years ago. Risk appears influenced by a more complex process involving genetic risk interfacing with multiple potentially interacting hits and vulnerability factors occurring at key periods of neurodevelopmental activity, which culminate in the expression of disease state. These risks are common across a number of neuropsychiatric and medical disorders, which might inform common preventive and intervention strategies across non-communicable disorders.

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Section: Prevention Strategiesmentioning

confidence: 99%

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

Davis

Eyre

Jacka

et al. 2016

Neuroscience & Biobehavioral Reviews

Self Cite

279

209

View full text Add to dashboard Cite

show abstract

“…A critical avenue is via service reform, especially the creation of early intervention services. They can also provide further impetus to study the efficacy of potential primary and secondary preventive strategies where evidence is so far scant. Education campaigns may help ill persons or those at risk to seek help in earlier stages, and service changes that welcome persons at earlier illness stages may lead more timely delivery of effective interventions.…”

Section: Implications and Directionsmentioning

confidence: 99%

Staging in bipolar disorder: from theoretical framework to clinical utility

et al. 2017

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Illness staging is widely utilized in several medical disciplines to help predict course or prognosis, and optimize treatment. Staging models in psychiatry in general, and bipolar disorder in particular, depend on the premise that psychopathology moves along a predictable path: an atrisk or latency stage, a prodrome progressing to a first clinical threshold episode, and one or more recurrences with the potential to revert or progress to late or end-stage manifestations. The utility and validity of a staging model for bipolar disorder depend on its linking to clinical outcome, treatment response and neurobiological measures. These include progressive biochemical, neuroimaging and cognitive changes, and potentially stage-specific differences in response to pharmacological and psychosocial treatments. Mechanistically, staging models imply the presence of an active disease process that, if not remediated, can lead to neuroprogression, a more malignant disease course and functional deterioration. Biological elements thought to be operative in bipolar disorder include a genetic diathesis, physical and psychic trauma, epigenetic changes, altered neurogenesis and apoptosis, mitochondrial dysfunction, inflammation, and oxidative stress. Many available agents, such as lithium, have effects on these targets. Staging models also suggest the utility of stage-specific treatment approaches that may not only target symptom reduction, but also impede illness neuroprogression. These treatment approaches range from prevention for at-risk individuals, to early intervention strategies for prodromal and newly diagnosed individuals, complex combination therapy for rapidly recurrent illness, and palliative-type approaches for those at chronic, late stages of illness. There is hope that prompt initiation of potentially disease modifying therapies may preclude or attenuate the cognitive and structural changes seen in the later stages of bipolar disorder. The aims of this paper are to: a) explore the current level of evidence supporting the descriptive staging of the syndromal pattern of bipolar disorder; b) describe preliminary attempts at validation; c) make recommendations for the direction of further studies; and d) provide a distillation of the potential clinical implications of staging in bipolar disorder within a broader transdiagnostic framework.

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“…The efficacy of cisplatin in the clinic is limited by severe side effects in some cases but more prominently by tumor resistance [8]. The side effects of cisplatin include nephrotoxicity, ototoxicity, neurotoxicity and other side effects common to chemotherapy [9], [10], [11].…”

Section: Introductionmentioning

confidence: 99%

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

2017

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Cisplatin is a widely used chemotherapeutic drug showing high efficiency in the treatment of primary tumors such as ovarian, testicular and cervical cancers. The major drawback of cisplatin is tumor resistance either acquired or intrinsic. Many mechanisms are involved in the resistance, among them is the Nrf2 pathway which regulates glutathione related enzymes. Caffeic acid, a non-toxic polyphenol which is abundant in many foods modulates glutathione S-transferase (GST) and glutathione reductase (GSR) activity, these enzymes were shown to be involved in resistance of cells towards cisplatin. Caffeic acid induces the Nrf2 pathway and can also inhibit the activity of GST and GSR.Our findings demonstrate that the co-treatment of cancer cells with cisplatin and caffeic acid can enhance cisplatin cytotoxicity and increases the amount of platinum bound to nuclear DNA. However, 6 h of pre incubation with caffeic acid prior to cisplatin treatment led to acquired resistance to cisplatin and reduced DNA binding.In conclusion, the enzyme inhibitory action of caffeic acid is dominant when the two agents are co-administered leading to increased cytotoxicity, and the Nrf2 induction is dominant when the cells are treated with caffeic acid prior to cisplatin treatment leading to resistance.The use of caffeic acid as adjuvant for cisplatin should be carefully examined due to different pharmacokinetic profiles of caffeic acid and cisplatin. Thus, it is questionable if the two agents can reach the tumors at the right time frame in vivo.

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A shared framework for the common mental disorders and Non-Communicable Disease: key considerations for disease prevention and control

Cited by 103 publications

References 34 publications

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

A review of vulnerability and risks for schizophrenia: Beyond the two hit hypothesis

Staging in bipolar disorder: from theoretical framework to clinical utility

The timing of caffeic acid treatment with cisplatin determines sensitization or resistance of ovarian carcinoma cell lines

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