To send content items to your account,
please confirm that you agree to abide by our usage policies.
If this is the first time you use this feature, you will be asked to authorise Cambridge Core to connect with your account.
Find out more about sending content to .
To send content items to your Kindle, first ensure email@example.com
is added to your Approved Personal Document E-mail List under your Personal Document Settings
on the Manage Your Content and Devices page of your Amazon account. Then enter the ‘name’ part
of your Kindle email address below.
Find out more about sending to your Kindle.
Note you can select to send to either the @free.kindle.com or @kindle.com variations.
‘@free.kindle.com’ emails are free but can only be sent to your device when it is connected to wi-fi.
‘@kindle.com’ emails can be delivered even when you are not connected to wi-fi, but note that service fees apply.
In Respiratory Syncytial Virus infection, the early identification of infants at risk for severe disease in order to potentially decrease morbidity could be considered a major goal. Current guidelines recommend only clinical observation for this purpose in infants without known comorbidities. However, recent evidence shows that the presence of pulmonary hypertension in this population is a relevant risk factor for the development of a severe illness, even in healthy infants. The determination of plasmatic NT-proBNP levels could help to identify those cases that benefit of echocardiographic screening to detect pulmonary hypertension in this population during hospitalization.
Folic acid (FA) supplementation is recommended in the periconceptional period, for the prevention of neural tube defects. Limited data are available on the folate status of New Zealand (NZ) pregnant women and its association with FA supplementation intake. Objectives were to examine the relationship between plasma folate (PF) and reported FA supplement use at 15 weeks’ gestation and to explore socio-demographic and lifestyle factors associated with PF. We used data and blood samples from NZ participants of the Screening for Pregnancy Endpoints cohort study. Healthy nulliparous women with singleton pregnancy (n 1921) were interviewed and blood samples collected. PF was analysed via microbiological assay. Of the participants, 73 % reported taking an FA supplement at 15 weeks’ gestation – of these, 79 % were taking FA as part of/alongside a multivitamin supplement. Of FA supplement users, 56 % reported consuming a daily dose of ≥800 μg; 39 % reported taking less than 400 µg/d. Mean PF was significantly higher in women reporting FA supplementation (54·6 (se 1·5) nmol/l) v. no FA supplementation (35·1 (se 1·6) nmol/l) (P<0·0001). Reported daily FA supplement dose and PF were significantly positively correlated (r 0·41; P<0·05). Younger maternal age, Pacific and Maori ethnicity and obesity were negatively associated with PF levels; vegetarianism was positively associated with PF. Reported FA supplement dose was significantly associated with PF after adjustment for socio-demographic, lifestyle confounders and multivitamin intake. The relationship observed between FA supplementation and PF demonstrates that self-reported intake is a reliable proxy for FA supplement use in this study population.
By investigating the survival and the biomarker detectability of a rock-inhabiting cyanobacterium, Chroococcidiopsis sp. CCMEE 029, the BIOMEX space experiment might contribute to a future exploitation of the Moon as a test-bed for key astrobiology tasks such as the testing of life-detection technologies and the study of life in space. Post-flight analyses demonstrated that the mixing of dried cells with sandstone and a lunar regolith simulant provided protection against space UV radiation. During the space exposure, dried cells not mixed with minerals were killed by 2.05 × 102 kJ m−2 of UV radiation, while cells mixed with sandstone or lunar regolith survived 1.59 × 102 and 1.79 × 102 kJ m−2, respectively. No differences in survival occurred among cells mixed and not mixed with minerals and exposed to space conditions in the dark; this finding suggests that space vacuum and 0.5 Gy of ionizing radiation did not impair the cells’ presence in space. The genomic DNA of dead cells was severely damaged but still detectable with PCR amplification of a short target, thus suggesting that short sequences should be targeted in a PCR-based approach when searching for traces of life. The enhanced stability of genomic DNA of dried cells mixed with minerals and exposed to space indicates that DNA might still be detectable after prolonged periods, possibly up to millions of years in microbes shielded by minerals. Overall, the BIOMEX results contribute to future experiments regarding the exposure of cells and their biomarkers to deep space conditions in order to further test the lithopanspermia hypothesis, the biomarker stability and the microbial endurance, with implications for planetary protection and to determine if the Moon has been contaminated during past human missions.
Variation in the CACNA1C gene has been associated with bipolar disorder in several genome-wide association studies. This gene encodes the alpha 1C subunit of L-type voltage-gated calcium channels, which play an essential role in neurons. We analysed 39 biomarkers in either cerebrospinal fluid or serum in relation to six different CACNA1C variants in 282 patients with bipolar disorder and 90 controls. We report associations of CACNA1C risk alleles with serum levels of BDNF as well as tissue plasminogen activator, which converts pro-BDNF to mature BDNF. This sheds light on links between CACNA1C genetic variants and pathophysiological mechanisms in bipolar disorder.
This study assessed whether S-100β protein could be measured in urine when detectable in plasma after a mild traumatic brain injury (mTBI). Clinical data, plasma and urine samples were collected for the 46 adult patients prospectively enrolled in the emergency department (ED) of a Level 1 trauma center. S-100β protein concentrations were analysed using ELISA. S-100β protein was detectable in 91% and 71% of plasma and urine samples, but values were not correlated (r = 0.002). Urine sampling would have been a non-invasive procedure, but it does not appear to be useful in the ED during the acute phase after an mTBI.
The Comprehensive Assessment of Neurodegeneration and Dementia (COMPASS-ND) cohort study of the Canadian Consortium on Neurodegeneration in Aging (CCNA) is a national initiative to catalyze research on dementia, set up to support the research agendas of CCNA teams. This cross-country longitudinal cohort of 2310 deeply phenotyped subjects with various forms of dementia and mild memory loss or concerns, along with cognitively intact elderly subjects, will test hypotheses generated by these teams.
The COMPASS-ND protocol, initial grant proposal for funding, fifth semi-annual CCNA Progress Report submitted to the Canadian Institutes of Health Research December 2017, and other documents supplemented by modifications made and lessons learned after implementation were used by the authors to create the description of the study provided here.
The CCNA COMPASS-ND cohort includes participants from across Canada with various cognitive conditions associated with or at risk of neurodegenerative diseases. They will undergo a wide range of experimental, clinical, imaging, and genetic investigation to specifically address the causes, diagnosis, treatment, and prevention of these conditions in the aging population. Data derived from clinical and cognitive assessments, biospecimens, brain imaging, genetics, and brain donations will be used to test hypotheses generated by CCNA research teams and other Canadian researchers. The study is the most comprehensive and ambitious Canadian study of dementia. Initial data posting occurred in 2018, with the full cohort to be accrued by 2020.
Availability of data from the COMPASS-ND study will provide a major stimulus for dementia research in Canada in the coming years.
It is becoming clear that post-traumatic stress disorder (PTSD) is not simply a psychiatric disorder, but one that involves pervasive physiological impairments as well. These physiological disturbances deserve attention in any attempt at integrative treatment of PTSD that requires a focus beyond the PTSD symptoms themselves. The physiological disturbances in PTSD range over many systems, but a common thread thought to underlie them is that the chronic effects of PTSD involve problems with allostatic control mechanisms that result in an excess in what has been termed “allostatic load” (AL). A pharmacological approach to reducing AL would be valuable, but, because of the large range of physiological issues involved – including metabolic, inflammatory, and cardiovascular systems – it is unclear whether there exists a simple comprehensive way to address the AL landscape. In this paper, we propose that the cannabinoid system may offer just such an approach, and we outline evidence for the potential utility of cannabinoids in reducing many of the chronic physiological abnormalities seen in PTSD which are thought to be related to excess AL.
To evaluate the association between novel pre- and post-operative biomarker levels and 30-day unplanned readmission or mortality after paediatric congenital heart surgery.
Children aged 18 years or younger undergoing congenital heart surgery (n = 162) at Johns Hopkins Hospital from 2010 to 2014 were enrolled in the prospective cohort. Collected novel pre- and post-operative biomarkers include soluble suppression of tumorgenicity 2, galectin-3, N-terminal prohormone of brain natriuretic peptide, and glial fibrillary acidic protein. A model based on clinical variables from the Society of Thoracic Surgery database was developed and evaluated against two augmented models.
Unplanned readmission or mortality within 30 days of cardiac surgery occurred among 21 (13%) children. The clinical model augmented with pre-operative biomarkers demonstrated a statistically significant improvement over the clinical model alone with a receiver-operating characteristics curve of 0.754 (95% confidence interval: 0.65–0.86) compared to 0.617 (95% confidence interval: 0.47–0.76; p-value: 0.012). The clinical model augmented with pre- and post-operative biomarkers demonstrated a significant improvement over the clinical model alone, with a receiver-operating characteristics curve of 0.802 (95% confidence interval: 0.72–0.89; p-value: 0.003).
Novel biomarkers add significant predictive value when assessing the likelihood of unplanned readmission or mortality after paediatric congenital heart surgery. Further exploration of the utility of these novel biomarkers during the pre- or post-operative period to identify early risk of mortality or readmission will aid in determining the clinical utility and application of these biomarkers into routine risk assessment.
The use of a proteomic approach to investigate changes in the milk proteome is growing and has parralleled the increasing technological developments in proteomics moving from early investigation using a gel-based two-dimensional separation approach to more quantitative method of current focus applying chromatography and mass spectrometry. Proteomic approaches to investigate lactational performance have made substantial findings especially in the alterations in lactation during mastitis. An experimental model of Streptococcus uberis infection of the mammary gland has been used as a means to determine change not only in the milk proteome, but also in the peptidome and in the metabolome caused by the infection. Examination of the peptidome, that is the peptides of less than 25 kDa in molecular weight, demonstrated an increase in small peptides most of which were casein degradation products but also included small bioactive peptides such as mammary-associated serum amyloid A3 (MSAA3). The peptidome has also been shown to differ depending on the causative bacteria of naturally occuring mastitis. The use of a non-gel-based relative quantitative proteomic methodology has revealed major changes in the protein component of milk in mastitis. The S. uberis infection lead to increases in the concentrations of proteins such as cathelicidins, haptoglobin, MSAA3 and decreases milk content of proteins such as xanthine oxidase, butyrophilin and β-1,4-galactosyltransferase. Analysis of all protein change data identified the acute phase, coagulation and complement pathways as well as proteins related to bile acid metabolism as being most modified. Examination of the small molecular weight organic molecules of milk using a metabolomic approach identified an increase in the content in milk during mastitis of bile acids such as taurochenodeoxycholic acid. Notable changes were also found in metabolites responding to infection of the mammary gland. Carbohydrate and nucleic acid metabolites were reduced, whereas lipid and nitrogen containing metabolites were increased. The latter included increases in amino acids along with di and tri peptides, likely to be the result of casein degradation. The use of proteomics and other omic technology is in its infancy in investigation of lactational parameters, but can already provide additional insight into the changes involved in disease and will have further value in physiological and nutritional investigation of lactation.
The purpose of this review is to consider the effects of the long-chain n-3 fatty acids found in marine foods, EPA and DHA, on risk for CVD, particularly fatal outcomes. It will examine both epidemiological and randomised controlled trial findings. The former studies usually examine associations between the dietary intake or the blood levels of EPA + DHA and CVD outcomes or, on occasion, total mortality. For example, our studies in the Framingham Heart Study and in the Women's Health Initiative Memory Study have demonstrated significant inverse relations between erythrocyte EPA + DHA levels (i.e. the Omega-3 Index) and total mortality. Recent data from the Cardiovascular Health Study reported the same relations between plasma phospholipid n-3 levels and overall healthy ageing. As regards randomised trials, studies in the 1990s and early 2000s were generally supportive of a cardiovascular benefit for fish oils (which contain EPA + DHA), but later trials were generally not able to duplicate these findings, at least for total CVD events. However, when restricted to effects on risk for fatal events, meta-analyses have shown consistent benefits for n-3 treatment. Taken together, the evidence is strong for a cardioprotective effect of EPA + DHA, especially when consumed in sufficient amounts to raise blood levels into healthy ranges. Establishing target EPA + DHA intakes to reduce risk for cardiovascular death is a high priority.
Non-communicable diseases (NCD) such as type-2 diabetes and CVD are now highly prevalent in both developed and developing countries. Evidence from both human and animal studies shows that early-life nutrition is an important determinant of NCD risk in later life. The mechanism by which the early-life environment influences future disease risk has been suggested to include the altered epigenetic regulation of gene expression. Epigenetic processes regulate the accessibility of genes to the cellular proteins that control gene transcription, determining where and when a gene is switched on and its level of activity. Epigenetic processes not only play a central role in regulating gene expression but also allow an organism to adapt to the environment. In this review, we will focus on how both maternal and paternal nutrition can alter the epigenome and the evidence that these changes are causally involved in determining future disease risk.
Dietary assessment methods including FFQ and food diaries are associated with many measurement errors including energy under-reporting and incorrect estimation of portion sizes. Such errors can lead to inconsistent results especially when investigating the relationship between food intake and disease causation. To improve the classification of a person's dietary intake and therefore clarify proposed links between diet and disease, reliable and accurate dietary assessment methods are essential. Dietary biomarkers have emerged as a complementary approach to the traditional methods, and in recent years, metabolomics has developed as a key technology for the identification of new dietary biomarkers. The objective of this review is to give an overview of the approaches used for the identification of biomarkers and potential use of the biomarkers. Over the years, a number of strategies have emerged for the discovery of dietary biomarkers including acute and medium term interventions and cross-sectional/cohort study approaches. Examples of the different approaches will be presented. Concomitant with the focus on single biomarkers of specific foods, there is an interest in the development of biomarker signatures for the identification of dietary patterns. In the present review, we present an overview of the techniques used in food intake biomarker discover, including the experimental approaches used and challenges faced in the field. While significant progress has been achieved in the field of dietary biomarkers in recent years, a number of challenges remain. Addressing these challenges will be key to ensure success in implementing use of dietary biomarkers.
Chronic inflammation is associated with disease risk and mortality in the general population. Soluble urokinase plasminogen activator receptor (suPAR) is a stable marker of chronic inflammation, and a higher serum-concentration of suPAR is found in individuals with an unhealthy lifestyle such as smoking. This article investigates the association between suPAR and dietary quality measured with the dietary quality score (DQS). The DQS is an index of the overall quality of an individual’s dietary habits assessed through a self-administered FFQ. Furthermore, this article investigates the association of both suPAR and the DQS with CVD risk and mortality in the general Danish population. We analysed 5347 individuals aged 30–60 years from the Danish Inter99 study cohort. Multiple linear regression analyses showed a linear inverse association between the DQS and suPAR (P=0·0005). Cox regression analyses showed an 18 (95 % CI 9, 26) % increase in the risk of death from any cause with each 1 ng/ml increase in suPAR. We found no significant association between the DQS and the mortality (hazard ratio: 1·16, 95 % CI 0·79, 1·69). All analyses were adjusted for demographics and lifestyle factors. The association between the DQS and suPAR on the one hand and suPAR and mortality on the other supports the argument that low dietary quality may constitute a health risk through its influence on chronic inflammation. Future research should examine whether suPAR is modifiable through changes in dietary habits.
Objectives: This report examined theta-band neurodynamics for potential biomarkers of brain health in athletes with concussion. Methods: Participants included college-age contact/collision athletes with (N=24) and without a history of concussion (N=16) in Study 1. Study 2 (N=10) examined changes over time in contact/collision athletes. There were two primary dependent variables: (1) theta-band phase-synchronization (e.g., functional connectivity) between medial and right-lateral electrodes; and (2) the within-subject correlation between synchronization strength on error trials and post-error reaction time (i.e., operationalization of cognitive control). Results: Head injury history was inversely related with medial-lateral connectivity. Head injury was also related to declines in a neurobehavioral measure of cognitive control (i.e., the single-trial relationship between connectivity and post-error slowing). Conclusions: Results align with a theory of connectivity-mediated cognitive control. Mild injuries undetectable by behavioral measures may still be apparent on direct measures of neural functioning. This report demonstrates that connectivity and cognitive control measures may be useful for tracking recovery from concussion. Theoretically relevant neuroscientific findings in healthy adults may have applications in patient populations, especially with regard to monitoring brain health. (JINS 2019, 25, 314–323)
Mild cognitive impairment (MCI) represents a transitional stage between healthy aging and dementia, and affects 10–15% of the population over the age of 65. The failure of drug trials in Alzheimer’s disease (AD) treatment has shifted researchers’ focus toward delaying progression from MCI to dementia, which would reduce the prevalence and costs of dementia profoundly. Diagnostic criteria for MCI increasingly emphasize the need for positive biomarkers to detect preclinical AD. The phenomenology of MCI comprises lower quality-of-life, greater symptoms of depression, and avoidant coping strategies including withdrawal from social engagement. Neurobiological features of MCI are hypoperfusion and hypometabolism in temporoparietal cortices, medial temporal lobe atrophy particularly in rhinal cortices, elevated tau and phosphorylated tau and decreased Aβ42 in cerebrospinal fluid, and brain Aβ42 deposition. Elevated tau can be identified in MCI, particularly in the entorhinal cortex, using positron emission tomography, and analysis of signal complexity using electroencephalography or magnetoencephalography holds promise as a biomarker. Assessment of MCI also relies on cognitive screening and neuropsychological assessment, but there is an urgent need for standardized cognitive tests to capitalize on recent discoveries in cognitive neuroscience that may lead to more sensitive measures of MCI. Cholinesterase inhibitors are frequently prescribed for MCI, despite the lack of evidence for their efficacy. Exercise and diet interventions hold promise for increasing reserve in MCI, and group psychoeducational programs teaching practical memory strategies appear effective. More work is needed to better understand the phenomenology and neurobiology of MCI, and how best to assess it and delay progression to dementia.
This study aimed to evaluate the longitudinal association of vitamin D status with glycaemia, insulin, homoeostatic model assessment of insulin resistance, adiponectin and leptin. A prospective cohort with 181 healthy, pregnant Brazilian women was followed at the 5th–13th, 20th–26th and 30th–36th gestational weeks. In this cohort, 25-hydroxyvitamin D (25(OH)D) plasma concentrations were analysed using liquid chromatography–tandem MS. Vitamin D status was categorised as sufficient or insufficient using the Endocrine Society Practice Guidelines (≥75/<75 nmol/l) and the Institute of Medicine (≥50/<50 nmol/l) thresholds. Linear mixed-effect regression models were employed to evaluate the association between vitamin D status and each outcome, considering interaction terms between vitamin D status and gestational age (P<0·1). At baseline, 70·7 % of pregnant women had 25(OH)D levels <75 nmol/l and 16 % had levels <50 nmol/l. Women with sufficient vitamin D status at baseline, using both thresholds, presented lower glycaemia than those with insufficient 25(OH)D. Pregnant women with 25(OH)D concentrations <75 nmol/l showed lower insulin (β=−0·12; 95 % CI −0·251, 0·009; P=0·069) and adiponectin (β=−0·070; 95 % CI −0·150, 0·010; P=0·085) concentrations throughout pregnancy than those with 25(OH)D levels ≥75 nmol/l. Pregnant women with 25(OH)D <50 nmol/l at baseline presented significantly higher leptin concentrations than those with 25(OH)D levels ≥50 nmol/l (β=−0·253; 95 % CI −0·044, 0·550; P=0·095). The baseline status of vitamin D influences the biomarkers involved in glucose metabolism. Vitamin D-sufficient women at baseline had higher increases in insulin and adiponectin changes throughout gestation than those who were insufficient.
In dairy cattle, resistance, tolerance and resilience refer to the adaptation ability to a broad range of environmental conditions, implying stable performances (e.g. production level, fertility status) independent from disease or infection pressure. All three mechanisms resistance, tolerance and resilience contribute to overall robustness, implying the evaluation of phenotyping and breeding strategies for improved robustness in dairy cattle populations. Classically, breeding approaches on improved robustness rely on simple production traits, in combination with detailed environmental descriptors and enhanced statistical modelling to infer possible genotype by environment interactions. In this regard, innovative environmental descriptors were heat stress indicators, and statistical modelling focussed on random regression or reaction norm methodology. A robust animal has high breeding values over a broad spectra of environmental levels. During the last years, direct health traits were included into selection indices, implying advances in genetic evaluations for traits being linked to resistance or tolerance against infectious and non-infectious diseases. Up to now, genetic evaluation for health traits is primarily based on subjectively measured producer-recorded data, with disease trait heritabilities in a low-to-moderate range. Thus, it is imperative to identify objectively measurable phenotypes as suitable biomarkers. New technologies (e.g. mid-infrared spectrometry) offer possibilities to determine potential biomarkers via laboratory analyses. Novel biomarkers include measurable physiological traits (e.g. serum metabolites, hormone levels) as indicators for a current infection, or the host’s reaction to environmental stressors. The rumen microbiome composition is proposed as a biomarker to detect interactions between host genotype and environmental effects. The understanding of host genetic variation in disease resistance and individual expression of robustness encourages analyses on the underlying immune response (IR) system. Recent advances have been made in order to infer the genetic background of IR traits and cows immunological competence in relation to functional and production traits. Thus, a last aspect of this review addresses the genetic background and current state of genetic control for resistance to economically relevant infectious and non-infectious dairy cattle diseases by considering immune-related factors.
Non-communicable diseases are projected to become the most common causes of death in Africa by 2030. The impact on health of epidemiological and nutritional transitions in sub-Saharan Africa remains unclear. To assess the trends of dietary fatty acids over time in Uganda, we examined fatty acids in serum collected from individuals in rural south-west Uganda, at three time points over two decades. Independent cross-sectional samples of 915 adults and children were selected from the general population cohort in 1990 (n 281), 2000 (n 283) and 2008 (n 351). Serum phospholipid fatty acids were measured by GC. Multivariate regression analyses were performed to compare the geometric means of fatty acids by time period. Serum fatty acid profiling showed high proportions of SFA, cis-MUFA and industrial trans-fatty acids (iTFA), likely to be biomarkers of high consumption of palm oil and hydrogenated fats. In contrast, proportions of n-6 and n-3 PUFA from vegetable oils and fish were low. From 1990 to 2008, serum phospholipids showed increases in absolute amounts of SFA (17·3 % increase in adults and 26·4 % in children), MUFA (16·7 % increase in adults and 16·8 % in children) and n-6:n-3 PUFA (40·1 % increase in adults and 39·8 % in children). The amount of elaidic acid, iTFA from hydrogenated fats, increased in children (60·1 % increase). In this rural Ugandan population, we show evidence of unfavourable trends over time of dietary fatty acids.
Individual biological predispositions should play a role in risky driving behaviour. Platelet monoamine oxidase (MAO) activity, dopamine transporter gene (DAT1) and neuropeptide S receptor 1 (NPSR1) gene polymorphisms have been identified as markers of impulsivity, alcohol use and excessive risk-taking. We aimed to find out how this knowledge on neurobiology of impulsivity applies to drunk driving and traffic behaviour in general.
We have longitudinally examined the behaviour of drunk drivers (n = 203) and controls (n = 211) in traffic, in association with their alcohol-related problems, personality measures and the three biomarkers. We analysed differences between the subjects based on whether they had committed driving while impaired by alcohol (DWI) violation in a 10-year time period after recruitment or not and investigated further, what kind of predictive value do the different biomarkers have in committing DWI and other traffic violations and accidents.
The original drunk drivers group had lower platelet MAO activity but further DWI was not significantly associated with this measure. Being a NPSR1 T-allele carrier contributed to the risk of repeatedly committing DWI. DAT1 9R carriers in contrast were involved in more traffic accidents by their own fault (active accidents), compared to 10R homozygotes in the whole sample. All groups with DWI also had significantly more alcohol-related problems and higher scores in maladaptive impulsivity compared to controls without DWI.
Established biological markers of alcohol use and impulsivity can be reliably associated with everyday traffic behaviour and help in contributing to the understanding of the need for more personalized prevention activities.
Enhanced sensitivity to oestrogen signalling may drive increased risk for depressive symptoms when exposed to peripartum sex-steroid hormone fluctuations.
Testing if 116 pre-identified sex steroid-responsive transcripts that predicted perinatal depression (PND) translates to a pharmacological model of hormone-induced mood changes.
We generated longitudinal, genome-wide gene-expression and DNA-methylation data from 60 women exposed to a gonadotrophin-releasing hormone agonist (GnRHa) or placebo. We used linear mixed-effect models to assess differences between baseline and follow-up for gene expression and DNA methylation in the biphasic ovarian response to GnRHa.
Of the 116 PND-predictive transcripts, a significant (19%) overlap was observed with those differentially expressed post-GnRHa at both early and later follow-up, indicating sustained effects. Similarly, 49% of tested genes were differentially methylated post-GnRHa at the late follow-up. Within the GnRHa group, a large proportion of PND genes were significantly associated (gene expression; DNA methylation) with changes in depressive symptoms (28%; 66%), oestradiol levels (49%; 66%) and neocortex serotonin transporter binding (8%; 45%) between baseline and follow-up.
Our data bridge clinical PND biomarkers with a pharmacological model of sex hormone-induced mood changes and directly relate oestrogen-induced biological changes with depressive symptoms and associated serotonin-signalling changes. Our data highlight that individual variations in molecular sensitivity to oestrogen associate with susceptibility to hormone-induced mood changes and hold promise for candidate biomarkers.
Declaration of interest
V.G.F. received honorarium for being a speaker for H. Lundbeck A/S. E.B.B. receives research funding from Böhringer Ingelheim to investigate FKBP5 as a potential drug target for depression.