Contact heat is commonly used in experimental research to evoke brain activity, most frequently acquired with electroencephalography (EEG). Although magnetoencephalography (MEG) improves spatial resolution, using some contact heat stimulators with MEG can present methodological challenges. This systematic review assesses studies that utilise contact heat in MEG, their findings and possible directions for further research.

Eight electronic databases were searched for relevant studies, in addition to the selected papers' reference lists, citations and ConnectedPapers maps. Best practice recommendations for systematic reviews were followed. Papers met inclusion criteria if they used MEG to record brain activity in conjunction with contact heat, regardless of stimulator equipment or paradigm.

Of 646 search results, seven studies met the inclusion criteria. Studies demonstrated effective electromagnetic artefact removal from MEG data, the ability to elicit affective anticipation and differences in deep brain stimulation responders. We identify contact heat stimulus parameters that should be reported in publications to ensure comparisons between data outcomes are consistent.

Contact heat is a viable alternative to laser or electrical stimulation in experimental research, and methods exist to successfully mitigate any electromagnetic noise generated by PATHWAY CHEPS equipment – though there is a dearth of literature exploring the post-stimulus time window.

Treatment-resistant depression (TRD) is the most problematic outcome of depression in terms of functional impairment, suicidal thoughts and decline in physical health.

To investigate the genetic predictors of TRD using a genome-wide approach to contribute to the development of precision medicine.

A sample recruited by the European Group for the Study of Resistant Depression (GSRD) including 1148 patients with major depressive disorder (MDD) was characterised for the occurrence of TRD (lack of response to at least two adequate antidepressant treatments) and genotyped using the Infinium PsychArray. Three clinically relevant patient groups were considered: TRD, responders and non-responders to the first antidepressant trial, thus outcomes were based on comparisons of these groups. Genetic analyses were performed at the variant, gene and gene-set (i.e. functionally related genes) level. Additive regression models of the outcomes and relevant covariates were used in the GSRD participants and in a fixed-effect meta-analysis performed between GSRD, STAR*D (n = 1316) and GENDEP (n = 761) participants.

No individual polymorphism or gene was associated with TRD, although some suggestive signals showed enrichment in cytoskeleton regulation, transcription modulation and calcium signalling. Two gene sets (GO:0043949 and GO:0000183) were associated with TRD versus response and TRD versus response and non-response to the first treatment in the GSRD participants and in the meta-analysis, respectively (corrected P = 0.030 and P = 0.027).

The identified gene sets are involved in cyclic adenosine monophosphate mediated signal and chromatin silencing, two processes previously implicated in antidepressant action. They represent possible biomarkers to implement personalised antidepressant treatments and targets for new antidepressants.

D.S. has received grant/research support from GlaxoSmithKline and Lundbeck; has served as a consultant or on advisory boards for AstraZeneca, Bristol-Myers Squibb, Eli Lilly, Janssen and Lundbeck. S.M. has been a consultant or served on advisory boards for: AstraZeneca, Bristol-Myers Squibb, Forest, Johnson & Johnson, Leo, Lundbeck, Medelink, Neurim, Pierre Fabre, Richter. S.K. has received grant/research support from Eli Lilly, Lundbeck, Bristol-Myers Squibb, GlaxoSmithKline, Organon, Sepracor and Servier; has served as a consultant or on advisory boards for AstraZeneca, Bristol-Myers Squibb, GlaxoSmithKline, Eli Lilly, Lundbeck, Pfizer, Organon, Schwabe, Sepracor, Servier, Janssen and Novartis; and has served on speakers' bureaus for AstraZeneca, Eli Lily, Lundbeck, Schwabe, Sepracor, Servier, Pierre Fabre, Janssen and Neuraxpharm. J.Z. has received grant/research support from Lundbeck, Servier, Brainsway and Pfizer, has served as a consultant or on advisory boards for Servier, Pfizer, Abbott, Lilly, Actelion, AstraZeneca and Roche and has served on speakers' bureaus for Lundbeck, Roch, Lilly, Servier, Pfizer and Abbott. J.M. is a member of the Board of the Lundbeck International Neuroscience Foundation and of Advisory Board of Servier. A.S. is or has been consultant/speaker for: Abbott, AbbVie, Angelini, Astra Zeneca, Clinical Data, Boehringer, Bristol Myers Squibb, Eli Lilly, GlaxoSmithKline, Innovapharma, Italfarmaco, Janssen, Lundbeck, Naurex, Pfizer, Polifarma, Sanofi and Servier. C.M.L. receives research support from RGA UK Services Limited.

Genetic studies of single gene variants have been criticized as providing a simplistic characterization of the genetic basis of illness risk that ignores the effects of other variants within the same biological pathways. Of candidate biological pathways for schizophrenia (SZ), the cell adhesion molecule (CAM) pathway has repeatedly been linked to both psychosis and neurocognitive dysfunction. Here we tested, using risk allele scores derived from the Schizophrenia Psychiatric Genome-Wide Association Study Consortium (PGC-SCZ), whether alleles within the CAM pathway were correlated with poorer neuropsychological function in patients.

In total, 424 patients with psychosis were assessed in areas of cognitive ability typically found to be impaired in SZ: intelligence quotient, memory, working memory and attentional control. CAM pathway genes were identified using the Kyoto Encyclopedia of Genes and Genomes (KEGG) database. Alleles within these genes identified as significantly associated with SZ risk in the PGC-SCZ were then used to calculate a CAM pathway-based polygenic risk allele score for each patient and these scores were tested for association with cognitive ability.

Increased CAM pathway polygenic risk scores were significantly associated with poorer performance on measures of memory and attention, explaining 1–3% of variation on these measures. Notably, the most strongly associated single nucleotide polymorphism (SNP) in the CAM pathway (rs9272105 within HLA-DQA1) explained a similar amount of variance in attentional control, but not memory, as the polygenic risk analysis.

These data support a role for the CAM pathway in cognitive function, both at the level of individual SNPs and the wider pathway. In so doing these data highlight the value of pathway-based polygenic risk score studies as well as single gene studies for understanding SZ-associated deficits in cognition.

To explore whether (direct) referrals from GPs to two Community Mental Health Team (CMHT) clinical psychologists differed from those received from both ‘Psychiatric’ (eg. consultant psychiatrists) and ‘Other’ sources.

The two psychologists retrospectively examined and coded the case files of all clients who attended them during a 12-month period. The six measures used were diagnostic prevalence and groups, co-morbidity, chronicity, previous hospital admission and CMHT contact Separate cross-tabulations and chi squared tests were conducted for the various dependent variables to profile differences across the three referral sources.

There was no difference in prevalence of Axis I disorders, co-morbidity and chronicity of disorders between ‘GP’ and ‘Psychiatric’ referrals to the two CMHT psychologists. However, although low in number, there were more eating and psychotic disorders among the ‘Psychiatric’ referrals, and more of these referrals had previous hospital admission and CMHT contact.

‘GP’ referrals were similar to ‘Psychiatric’ referrals on some measures but differed on others. Hence, as to whether an ‘open access’ model of (direct) referral to CMHT clinical psychologists lowers the clinical threshold for referrals depends on which measures are deemed most critical. Consistently applying a composite index of referral ‘severity’ could prevent the former.