Methylphenidate (MPD) is a drug prescribed for the treatment of attention deficit/hyperactivity disorder and its therapeutic effect is attributed to the inhibition of dopamine.

Young male Wistar rats were administered MPD (1, 2, 5, or 10 mg/kg) once a day or an intraperitoneal injection of saline for 28 days (chronic treatment) or for 1 day (acute treatment). Two hours after the last administration the animals were decapitated and their striatum was dissected.

In this work, we show that continued treatment with MPD is capable of modifying the levels of phosphorylation of proteins JNK1/2 (c-Jun amino-terminal kinases 1 and 2) and ERK1/2 (extracellular signal-regulated kinases 1 and 2). Whereas the level of phosphorylation of protein ERK increased significantly, that of proteins JNK1/2 diminished.

The alteration in the level of activation of mitogen-activated protein kinases can be a molecular mechanism through which MPD exerts its therapeutic effect.

We investigated the relationship of oestrogen receptor (ER) status to the severity of depressive symptoms and quality of life (QOL) impairment in breast cancer patients.

Seventy-seven breast cancer patients with comorbid depression were evaluated with the Hamilton Depression Rating Scale (HAMD), the Clinical Global Impression-Severity of Illness (CGI-S) for depression, and the Functional Assessment of Cancer Therapy-Breast (FACT-B). ER status was determined using immunohistochemical analysis.

The ER-positive group (n = 31) showed significantly higher scores compared with the ER-negative group (n = 46) on HAMD total (p = 0.04) and somatic anxiety factor (p = 0.004) scores as well as CGI-S score (p = 0.03). As for QOL measured with the FACT-B, a significantly higher score was found on the Functional Well-Being (FWB) subscale in the ER-positive group (p = 0.001). The relationships were further analysed using generalised linear models (GLM), after controlling for the influence of the current anti-oestrogen treatment. The analysis revealed that ER status was still significantly related to the FWB subscale score of the FACT-B (p = 0.04). However, the HAMD and CGI-S scores were no longer significantly related to ER status after the influence of anti-oestrogen treatment was controlled for.

These results suggest that ER status, which is a well-known biological prognostic factor in breast cancer, may be related to the severity of certain aspects of depressive symptoms or QOL impairment, implying a role of the ER in affective and behavioural regulation. However, anti-oestrogen treatments significantly influence these relationships.

Comparing schizophrenia patients on the basis of familial and non-familial forms of the illness provides a promising approach to the identification of genes involved in schizophrenia. The aim of this study was to search for somatic factors that discriminate between patients with and without a family history of schizophrenia and between their relatives.

Ninety-five schizophrenia patients were structurally interviewed about mental and physical health and alcohol and substance use in themselves and their families. Besides this, complementary information was obtained from the patients’ case records. Patients with (41%) and without (59%) a family history were then compared.

The main differences were found in the patients’ relatives. Fewer patients with a family history, compared with patients without a family history, had relatives with cancer (p = 0.002). Conversely, there was a tendency towards that more patients with a family history, compared with patients without a family history, had relatives with cardiac infarction (p = 0.05).

The genetic risk associated with schizophrenia seems to cosegregate into a factor(s) that protects against cancer and possibly also increases the risk for cardiac infarction.

The cause of cognitive side effects after electroconvulsive therapy (ECT) is largely unknown. Alterations in the blood–brain barrier (BBB) have been considered in several recent ECT studies. We therefore found it worthwhile to perform a systematic review of the literature to examine if electrically induced seizures affect the permeability of the BBB.

PubMed/MEDLINE and Embase were searched 16 November 2022. Studies with a direct measurement of BBB permeability in animals treated with modified electroconvulsive stimulation (ECS) and in humans treated with ECT were included. Synthesis of results was narrative due to the low number of studies and differences in study designs.

Four animal and two human (31 participants) studies were included. In animals, two studies found increased BBB permeability to some smaller molecules after modified ECS, while the two other studies found marginally increased or unchanged permeability to albumin after treatment. In contrast, the human studies did not find increased BBB permeability to smaller molecules or albumin after ECT.

Animal but not human studies support increased BBB permeability to some smaller molecules after electrically induced seizures. However, this conclusion is confined by the low number of studies and the lack of studies applying state-of-the-art methods. More studies using modern approaches to measuring of BBB permeability are warranted.

The study was founded by Mental Health Services in the Capital Region of Denmark (grant number 61151-05) and was registered on PROSPERO before data extraction was initiated (CRD42022331385).

The perception of music without a stimulus, or musical hallucination, is reported in both organic and psychiatric disorders. It is most frequently described in the elderly with associated hearing loss and accompanied by some degree of insight. In this setting it is often referred to as ‘musical hallucinosis’. The aim of the authors was to present examples of this syndrome and review the current understanding of its neurobiological basis.

We describe three cases of persons experiencing musical hallucinosis in the context of hearing deficits with varying degrees of associated central nervous system abnormalities.

Putative neurobiological mechanisms, in particular those involving de-afferentation of a complex auditory recognition system by complete or partial deafness, are discussed in the light of current information from the literature.

Musical hallucinosis can be experienced in those patients with hearing impairment and is phenomenologically distinct for hallucinations described in psychiatric disorders.

Recognition memory dysfunction has been frequently reported in schizophrenic populations, and has been linked with the development of delusions and thought disorder. A range of neuropsychological abnormalities have also been documented in the biological asymptomatic relatives of patients with schizophrenia; however, recognition memory has not been one of them.

This study was carried out in order to investigate: (i) verbal and facial recognition memory in terms of accuracy and false alarm rates; and (ii) contributions from the episodic and semantic memory systems to recognition memory, in the biological asymptomatic parents of a reported schizophrenic patient and a set of male and female psychotic controls.

Gender differences failed to emerge between the psychotic controls on any of the recognition measures (discrimination accuracy, response bias, hit and false alarm rates, ‘remember’ and ‘know’ recognition memory decisions). However, there was evidence of recognition dysfunction in the female relative, and to a lesser extent, in the male. Both parent's recognition memory performance profiles were marked by a pathologically elevated false alarm rate, and an increased dependence ‘remember’ judgements, i.e. input from the episodic memory system, to drive recognition memory decisions.

These findings are discussed in the context of models of episodic and semantic memory impairment in schizophrenia.

Identification of candidate genes for schizophrenia may be more successful than genome screens as the latter have not found consistent linkages.

To assist in the gene search, a model of schizophrenia based on resistance to infectious diseases, rather than susceptibility, is proposed. The theory blends the geography of schizophrenia with the assumption that genes that cause schizophrenia likely evolved and persist from selection pressure. The theory includes the notion that schizophrenia enhances biological survival at the cost of psychological and social functioning.

To demonstrate the utility of using this model, the Medline literature was searched for resistance genes, mostly identified in mice.

Based on homologous locations in the human genome, these resistance genes are shown to be located in human chromosome regions linked significantly, in at least one genome screen, with schizophrenia or some physiologically related function or condition associated with schizophrenia.

The infectious disease resistance theory of schizophrenia is offered as a viable model for understanding the origins of schizophrenia. The theory also allows for the inclusion of persistent infections, seasonal variability and translational pathophysiology to contribute to the etiology of schizophrenia.