Ste. Anne's Hospital (French: Hôpital Sainte-Anne) is a hospital located in Sainte-Anne-de-Bellevue, Quebec, Canada. It primarily serves veterans of the Canadian Forces and is specialized in long-term and geriatric care. It also treats younger veterans for operational stress injuries and post-traumatic stress disorder. The hospital has 446 beds in private rooms and underwent an extensive renovation in 2009.
OBJECTIVES:This World Federation of Societies of Biological Psychiatry (WFSBP) consensus paper aims to summarise and evaluate the published study results on objectively measurable biological markers associated with anorexia nervosa (AN). METHODS:The relevant literature was reviewed by the WFSBP Task Forces on Eating Disorders and on Biological Markers, and a consensus regarding the significance of the published evidence was reached. RESULTS:Candidate biological markers that have been associated with AN include clinical (e.g. body weight), molecular (e.g. genetic, epigenetic, hormonal, immunological, metabolomic), cellular (e.g. leukocytes), neuroimaging (e.g. structure, function, connectivity), digital, cardiac and neurophysiological parameters. Some clinical and laboratory parameters are risk markers in clinical practice. Biological markers have pathophysiological relevance in understanding the biological and metabolic pathophysiology of AN and its physical health consequences. Few studies have examined pharmacogenetics or therapeutic drug monitoring as tools to monitor and guide the treatment of AN. CONCLUSIONS:Biological markers will hopefully soon enable clinicians to intervene earlier in a more targeted manner to mitigate treatment resistance. However, the current scientific basis for most biological markers are group comparisons only. Studies on sensitivity, specificity and the prognostic value of these markers are lacking.
Over the last four decades, studies provided evidence that individuals tend to rate statements as being more truthful when they are re-exposed to them, the so-called 'illusory truth effect'. In light of a growing number of studies published since the previous meta-analysis in 2006 and concern of publishing biases, we conduct a meta-analysis on 182 studies and 366 effect sizes (N = 31,184 participants) published from 1977 to 2025. After correcting for small-study effects, we observe a small illusory truth effect (g = 0.37, 95% confidence interval [0.30, 0.44]), with a substantial within and between-study heterogeneity. Here, we show that multiple variables accounted for such heterogeneity, including the type of item, the instructions during the first exposure, the presence of veracity cues, and the duration of presentation on first exposure to the statement. We highlight the importance of the initial exposure and discuss practical implications regarding the current misinformation crisis.
Burnout syndrome (BOS) represents an enduring challenge for preventive medicine. While biomarkers of chronic stress have been explored within the allostatic load framework, BOS lacks a consistent physiological signature, hindering early and comprehensive identification of individuals at risk. This systematic review synthesises current evidence on BOS-related biomarkers, aiming to identify potential physiological correlates. We conducted a comprehensive search of PubMed and EMBASE, yielding 111 studies evaluating 36 biomarkers in adult populations. Our analysis revealed inconsistent associations across most physiological systems, including the hypothalamic-pituitary-adrenal axis (e.g., cortisol, DHEA), the immune system, and cardiovascular parameters. While some biomarkers such as HbA1c and blood glucose showed relatively more consistent associations with BOS, the overall findings remain largely inconclusive. Overall, the current biological evidence is insufficient to identify a BOS biosignature that could support routine clinical diagnosis. Future research should prioritise a more unified and comprehensive definition of BOS and investigate physiological patterns within more standardized research frameworks to advance objective identification and prevention strategies.
Abstract Herpes Simplex virus type 1 (HSV-1) is a highly prevalent neurotropic virus from the alphaherpesviruses family. In recent years, a growing body of research has focused on the potential role of HSV-1 infections and recurrent reactivations in the pathophysiology of Alzheimer’s disease (AD). In particular, it has been hypothesized that HSV-1 could initiate or amplify the formation of neuropathological lesions characteristic of AD. To explore further this hypothesis, we adopted an integrated approach aiming at deciphering the impact of HSV-1 infection on AD molecular markers (Aß and Tau pathologies) and combining experimental animal models of in vivo infection, postmortem neuropathological analysis of AD brains, as well as in-vivo clinical analysis in AD patients. In animal models of peripheral (labial) infection with HSV-1 virus, we analyzed viral dissemination from peripheral tissues to the CNS, and the associated neuropathological consequences. Histological and molecular analyses revealed the occurrence of viral material (RNA, proteins) in the brainstem, the primary site of viral neuroinvasion, and in more anterior regions of the brain. Viral signatures were accompanied by early abnormal deposits of Aβ peptides and accumulation of phosphoTau (pTau) proteins in various brain areas. Neuropathological examination of AD/control participants also underlined the presence of HSV-1 DNA in the human brainstem (pons) that was always associated with local Aß/Tau aggregates. Finally, in AD patients, associations were found between HSV-1 seropositivity and neuropathological lesion burden (region-specific Tau and Aβ deposition detected by neuroimaging). Taken together, these data provide new evidence in favor of the involvement of HSV-1 in the pathophysiology of AD, stressing a possible causal link between HSV-1 infection, neuroinvasion and AD neuropathological hallmarks (Aß lesions and tauopathy).
