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Article ; Online: Persistent thinness and anorexia nervosa differ on a genomic level.

Hübel, Christopher / Abdulkadir, Mohamed / Herle, Moritz / Palmos, Alish B / Loos, Ruth J F / Breen, Gerome / Micali, Nadia / Bulik, Cynthia M

European journal of human genetics : EJHG

2023 Volume 32, Issue 1, Page(s) 117–124

Abstract: Thinness and anorexia nervosa are both characterised by persistent low weight. Individuals with anorexia nervosa concurrently report distorted perceptions of their body and engage in weight-loss behaviours, whereas individuals with thinness often wish to ...

Abstract	Thinness and anorexia nervosa are both characterised by persistent low weight. Individuals with anorexia nervosa concurrently report distorted perceptions of their body and engage in weight-loss behaviours, whereas individuals with thinness often wish to gain weight. Both conditions are heritable and share genomics with BMI, but are not genetically correlated with each other. Based on their pattern of genetic associations with other traits, we explored differences between thinness and anorexia nervosa on a genomic level. In Part 1, using publicly available data, we compared genetic correlations of persistent thinness/anorexia nervosa with eleven psychiatric disorders. In Part 2, we identified individuals with adolescent persistent thinness in the Avon Longitudinal Study of Parents and Children (ALSPAC) by latent class growth analysis of measured BMI from 10 to 24 years (n = 6594) and evaluated associations with psychiatric and anthropometric polygenic scores. In Part 1, in contrast to the positive genetic correlations of anorexia nervosa with various psychiatric disorders, persistent thinness showed negative genetic correlations with attention deficit hyperactivity disorder (r
MeSH term(s)	Adolescent ; Child ; Humans ; Anorexia Nervosa/genetics ; Anorexia Nervosa/psychology ; Depressive Disorder, Major ; Thinness/genetics ; Longitudinal Studies ; Genomics
Language	English
Publishing date	2023-07-20
Publishing country	England
Document type	Journal Article
ZDB-ID	1141470-4
ISSN	1476-5438 ; 1018-4813
ISSN (online)	1476-5438
ISSN	1018-4813
DOI	10.1038/s41431-023-01431-8
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Zs.A 3589: Show issues

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Article ; Online: Genetics of eating disorders in the genome-wide era.

Watson, Hunna J / Palmos, Alish B / Hunjan, Avina / Baker, Jessica H / Yilmaz, Zeynep / Davies, Helena L

Psychological medicine

2021 Volume 51, Issue 13, Page(s) 2287–2297

Abstract: Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic ... ...

Abstract	Enabled by advances in high throughput genomic sequencing and an unprecedented level of global data sharing, molecular genetic research is beginning to unlock the biological basis of eating disorders. This invited review provides an overview of genetic discoveries in eating disorders in the genome-wide era. To date, five genome-wide association studies on eating disorders have been conducted - all on anorexia nervosa (AN). For AN, several risk loci have been detected, and ~11-17% of the heritability has been accounted for by common genetic variants. There is extensive genetic overlap between AN and psychological traits, especially obsessive-compulsive disorder, and intriguingly, with metabolic phenotypes even after adjusting for body mass index (BMI) risk variants. Furthermore, genetic risk variants predisposing to lower BMI may be causal risk factors for AN. Causal genes and biological pathways of eating disorders have yet to be elucidated and will require greater sample sizes and statistical power, and functional follow-up studies. Several studies are underway to recruit individuals with bulimia nervosa and binge-eating disorder to enable further genome-wide studies. Data collections and research labs focused on the genetics of eating disorders have joined together in a global effort with the Psychiatric Genomics Consortium. Molecular genetics research in the genome-wide era is improving knowledge about the biology behind the established heritability of eating disorders. This has the potential to offer new hope for understanding eating disorder etiology and for overcoming the therapeutic challenges that confront the eating disorder field.
MeSH term(s)	Anorexia Nervosa/genetics ; Bulimia Nervosa/genetics ; Feeding and Eating Disorders/epidemiology ; Feeding and Eating Disorders/genetics ; Genome-Wide Association Study ; Genomics ; Humans ; Molecular Biology ; Phenotype
Language	English
Publishing date	2021-02-15
Publishing country	England
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't ; Review
ZDB-ID	217420-0
ISSN	1469-8978 ; 0033-2917
ISSN (online)	1469-8978
ISSN	0033-2917
DOI	10.1017/S0033291720005474
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Article ; Online: Assessing the Evidence for Causal Associations Between Body Mass Index, C-Reactive Protein, Depression, and Reported Trauma Using Mendelian Randomization.

Palmos, Alish B / Hübel, Christopher / Lim, Kai Xiang / Hunjan, Avina K / Coleman, Jonathan R I / Breen, Gerome

Biological psychiatry global open science

2022 Volume 3, Issue 1, Page(s) 110–118

Abstract: Background: Traumatic experiences are described as the strongest predictors of major depressive disorder (MDD), with inflammation potentially mediating the association between trauma and symptom onset. However, several studies indicate that body mass ... ...

Abstract	Background: Traumatic experiences are described as the strongest predictors of major depressive disorder (MDD), with inflammation potentially mediating the association between trauma and symptom onset. However, several studies indicate that body mass index (BMI) exerts a large confounding effect on both inflammation and MDD. Methods: First, we sought to replicate previously reported associations between these traits in a large subset of the UK Biobank, using regression models with C-reactive protein (CRP) and MDD and as the outcome variables in 113,481 and 30,137 individuals, respectively. Second, we ran bidirectional Mendelian randomization analyses between these traits to establish a potential causal framework between BMI, MDD, reported childhood trauma, and inflammation. Results: Our phenotypic analyses revealed no association between CRP and MDD but did suggest a strong effect of BMI and reported trauma on both CRP (BMI: β = 0.43, 95% CI = 0.43-0.43, Conclusions: Our findings highlight the importance of controlling for both BMI and trauma when studying MDD in the context of inflammation. They also suggest that the experience of traumatic events can increase the risk for MDD and that MDD can increase the experience of traumatic events.
Language	English
Publishing date	2022-01-28
Publishing country	United States
Document type	Journal Article
ISSN	2667-1743
ISSN (online)	2667-1743
DOI	10.1016/j.bpsgos.2022.01.003
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Article ; Online: Lithium treatment and human hippocampal neurogenesis.

Palmos, Alish B / Duarte, Rodrigo R R / Smeeth, Demelza M / Hedges, Erin C / Nixon, Douglas F / Thuret, Sandrine / Powell, Timothy R

Translational psychiatry

2021 Volume 11, Issue 1, Page(s) 555

Abstract: Lithium is a first-line treatment for bipolar disorder, where it acts as a mood-stabilizing agent. Although its precise mechanism remains unclear, neuroimaging studies have shown that lithium accumulates in the hippocampus and that chronic use amongst ... ...

Abstract	Lithium is a first-line treatment for bipolar disorder, where it acts as a mood-stabilizing agent. Although its precise mechanism remains unclear, neuroimaging studies have shown that lithium accumulates in the hippocampus and that chronic use amongst bipolar disorder patients is associated with larger hippocampal volumes. Here, we tested the chronic effects of low (0.75 mM) and high (2.25 mM) doses of lithium on human hippocampal progenitor cells and used immunocytochemistry to investigate the effects of lithium on cell parameters implicated in neurogenesis. Corresponding RNA-sequencing and gene-set enrichment analyses were used to evaluate whether genes affected by lithium in our model overlap with those regulating the volume of specific layers of the dentate gyrus. We observed that high-dose lithium treatment in human hippocampal progenitors increased the generation of neuroblasts (P ≤ 0.01), neurons (P ≤ 0.01), and glia (P ≤ 0.001), alongside the expression of genes, which regulate the volume of the molecular layer of the dentate gyrus. This study provides empirical support that adult hippocampal neurogenesis and gliogenesis are mechanisms that could contribute to the effects of lithium on human hippocampal volume.
MeSH term(s)	Dentate Gyrus ; Hippocampus ; Humans ; Lithium ; Lithium Compounds/pharmacology ; Neurogenesis ; Neurons
Chemical Substances	Lithium Compounds ; Lithium (9FN79X2M3F)
Language	English
Publishing date	2021-10-30
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-021-01695-y
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Article ; Online: Proteome-wide Mendelian randomization identifies causal links between blood proteins and severe COVID-19.

Palmos, Alish B / Millischer, Vincent / Menon, David K / Nicholson, Timothy R / Taams, Leonie S / Michael, Benedict / Sunderland, Geraint / Griffiths, Michael J / Hübel, Christopher / Breen, Gerome

PLoS genetics

2022 Volume 18, Issue 3, Page(s) e1010042

Abstract: In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for ...

Abstract	In November 2021, the COVID-19 pandemic death toll surpassed five million individuals. We applied Mendelian randomization including >3,000 blood proteins as exposures to identify potential biomarkers that may indicate risk for hospitalization or need for respiratory support or death due to COVID-19, respectively. After multiple testing correction, using genetic instruments and under the assumptions of Mendelian Randomization, our results were consistent with higher blood levels of five proteins GCNT4, CD207, RAB14, C1GALT1C1, and ABO being causally associated with an increased risk of hospitalization or respiratory support/death due to COVID-19 (ORs = 1.12-1.35). Higher levels of FAAH2 were solely associated with an increased risk of hospitalization (OR = 1.19). On the contrary, higher levels of SELL, SELE, and PECAM-1 decrease risk of hospitalization or need for respiratory support/death (ORs = 0.80-0.91). Higher levels of LCTL, SFTPD, KEL, and ATP2A3 were solely associated with a decreased risk of hospitalization (ORs = 0.86-0.93), whilst higher levels of ICAM-1 were solely associated with a decreased risk of respiratory support/death of COVID-19 (OR = 0.84). Our findings implicate blood group markers and binding proteins in both hospitalization and need for respiratory support/death. They, additionally, suggest that higher levels of endocannabinoid enzymes may increase the risk of hospitalization. Our research replicates findings of blood markers previously associated with COVID-19 and prioritises additional blood markers for risk prediction of severe forms of COVID-19. Furthermore, we pinpoint druggable targets potentially implicated in disease pathology.
MeSH term(s)	Biomarkers/analysis ; Biomarkers/blood ; Blood Proteins/analysis ; Blood Proteins/genetics ; Blood Proteins/metabolism ; COVID-19/blood ; COVID-19/diagnosis ; COVID-19/mortality ; COVID-19/pathology ; Causality ; Genome-Wide Association Study ; Hospitalization ; Humans ; Mendelian Randomization Analysis ; Mortality ; Pandemics ; Polymorphism, Single Nucleotide ; Prognosis ; Proteome/analysis ; Proteome/genetics ; Proteome/metabolism ; Respiratory Insufficiency/blood ; Respiratory Insufficiency/diagnosis ; Respiratory Insufficiency/mortality ; Respiratory Insufficiency/pathology ; Risk Factors ; SARS-CoV-2/physiology ; Severity of Illness Index
Chemical Substances	Biomarkers ; Blood Proteins ; Proteome
Language	English
Publishing date	2022-03-03
Publishing country	United States
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	2186725-2
ISSN	1553-7404 ; 1553-7390
ISSN (online)	1553-7404
ISSN	1553-7390
DOI	10.1371/journal.pgen.1010042
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Article ; Online: Telomere length and human hippocampal neurogenesis.

Palmos, Alish B / Duarte, Rodrigo R R / Smeeth, Demelza M / Hedges, Erin C / Nixon, Douglas F / Thuret, Sandrine / Powell, Timothy R

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2020 Volume 45, Issue 13, Page(s) 2239–2247

Abstract: Short telomere length is a risk factor for age-related disease, but it is also associated with reduced hippocampal volumes, age-related cognitive decline and psychiatric disorder risk. The current study explored whether telomere shortening might have an ... ...

Abstract	Short telomere length is a risk factor for age-related disease, but it is also associated with reduced hippocampal volumes, age-related cognitive decline and psychiatric disorder risk. The current study explored whether telomere shortening might have an influence on cognitive function and psychiatric disorder pathophysiology, via its hypothesised effects on adult hippocampal neurogenesis. We modelled telomere shortening in human hippocampal progenitor cells in vitro using a serial passaging protocol that mimics the end-replication problem. Serially passaged progenitors demonstrated shorter telomeres (P ≤ 0.05), and reduced rates of cell proliferation (P ≤ 0.001), with no changes in the ability of cells to differentiate into neurons or glia. RNA-sequencing and gene-set enrichment analyses revealed an effect of cell ageing on gene networks related to neurogenesis, telomere maintenance, cell senescence and cytokine production. Downregulated transcripts in our model showed a significant overlap with genes regulating cognitive function (P ≤ 1 × 10
MeSH term(s)	Adult ; Bipolar Disorder ; Cellular Senescence ; Hippocampus ; Humans ; Neurogenesis ; Telomere ; Telomere Shortening
Language	English
Publishing date	2020-09-13
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-020-00863-w
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Article ; Online: Reconsidering the reasons for heightened inflammation in major depressive disorder.

Palmos, Alish B / Chung, Raymond / Frissa, Souci / Goodwin, Laura / Hotopf, Matthew / Hatch, Stephani L / Breen, Gerome / Powell, Timothy R

Journal of affective disorders

2020 Volume 282, Page(s) 434–441

Abstract: Background: Increased circulating pro-inflammatory markers have repeatedly been associated with major depressive disorder (MDD). However, it remains unclear whether inflammation represents a causal mechanism for MDD, or whether the association is ... ...

Abstract	Background: Increased circulating pro-inflammatory markers have repeatedly been associated with major depressive disorder (MDD). However, it remains unclear whether inflammation represents a causal mechanism for MDD, or whether the association is influenced by confounding factors such as body mass index (BMI). Methods: To better understand this complex relationship, we generated polygenic risk scores (PRS) for MDD and BMI in a population cohort and attempted to isolate the impact these potential risk factors have on adulthood inflammation. Peripheral blood samples were collected as part of the South East London Community Health study, where we generated individualized PRS for MDD and BMI and quantified inflammatory markers using multiplex ELISA-based technology. We performed linear regressions to investigate the effects of PRS for MDD and BMI on inflammatory marker levels. Results: Out of 35 inflammatory markers, we found a nominal effect of PRS for MDD on interleukin-10. We also found a significant positive effect of BMI on nine inflammatory markers, of which the two most strongly affected markers, interleukin-6 (IL-6) and C-reactive protein (CRP), were also nominally predicted by BMI PRS. Limitations: The study utilized a cross-sectional design with a moderately sized sample. Conclusions: Our findings suggest there may not be a shared genetic mechanism contributing to MDD and higher inflammatory marker levels. However, there may be shared genetic etiology between BMI and adulthood levels of CRP and IL-6. Therefore, polygenic risk scores for BMI may represent a useful indicator for heightened levels of inflammation in adulthood.
MeSH term(s)	Adult ; Cross-Sectional Studies ; Depressive Disorder, Major/genetics ; Humans ; Inflammation/genetics ; London ; Multifactorial Inheritance
Language	English
Publishing date	2020-12-28
Publishing country	Netherlands
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	135449-8
ISSN	1573-2517 ; 0165-0327
ISSN (online)	1573-2517
ISSN	0165-0327
DOI	10.1016/j.jad.2020.12.109
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Article: Genetic Risk for Psychiatric Disorders and Telomere Length.

Palmos, Alish B / Breen, Gerome / Goodwin, Laura / Frissa, Souci / Hatch, Stephani L / Hotopf, Matthew / Thuret, Sandrine / Lewis, Cathryn M / Powell, Timothy R

Frontiers in genetics

2018 Volume 9, Page(s) 468

Abstract: Background: ...

Abstract	Background:
Language	English
Publishing date	2018-10-16
Publishing country	Switzerland
Document type	Journal Article
ZDB-ID	2606823-0
ISSN	1664-8021
ISSN	1664-8021
DOI	10.3389/fgene.2018.00468
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Article ; Online: The polygenic nature of telomere length and the anti-ageing properties of lithium.

Coutts, Fiona / Palmos, Alish B / Duarte, Rodrigo R R / de Jong, Simone / Lewis, Cathryn M / Dima, Danai / Powell, Timothy R

Neuropsychopharmacology : official publication of the American College of Neuropsychopharmacology

2018 Volume 44, Issue 4, Page(s) 757–765

Abstract: Telomere length is a promising biomarker for age-related disease and a potential anti-ageing drug target. Here, we study the genetic architecture of telomere length and the repositioning potential of lithium as an anti-ageing medication. LD score ... ...

Abstract	Telomere length is a promising biomarker for age-related disease and a potential anti-ageing drug target. Here, we study the genetic architecture of telomere length and the repositioning potential of lithium as an anti-ageing medication. LD score regression applied to the largest telomere length genome-wide association study to-date, revealed SNP-chip heritability estimates of 7.29%, with polygenic risk scoring capturing 4.4% of the variance in telomere length in an independent cohort (p = 6.17 × 10
MeSH term(s)	Adult ; Animals ; Bipolar Disorder/drug therapy ; Bipolar Disorder/genetics ; Caenorhabditis elegans ; Case-Control Studies ; Female ; Gene Expression/drug effects ; Genome-Wide Association Study ; Humans ; Lithium/pharmacology ; Longevity/drug effects ; Male ; Middle Aged ; Telomere/drug effects ; Telomere/genetics
Chemical Substances	Lithium (9FN79X2M3F)
Language	English
Publishing date	2018-12-18
Publishing country	England
Document type	Journal Article ; Research Support, Non-U.S. Gov't
ZDB-ID	639471-1
ISSN	1740-634X ; 0893-133X
ISSN (online)	1740-634X
ISSN	0893-133X
DOI	10.1038/s41386-018-0289-0
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Article ; Online: Estradiol reverses excitatory synapse loss in a cellular model of neuropsychiatric disorders.

Erli, Filippo / Palmos, Alish B / Raval, Pooja / Mukherjee, Jayanta / Sellers, Katherine J / Gatford, Nicholas J F / Moss, Stephen J / Brandon, Nicholas J / Penzes, Peter / Srivastava, Deepak P

Translational psychiatry

2020 Volume 10, Issue 1, Page(s) 16

Abstract: Loss of glutamatergic synapses is thought to be a key cellular pathology associated with neuropsychiatric disorders including schizophrenia (SCZ) and major depressive disorder (MDD). Genetic and cellular studies of SCZ and MDD using in vivo and in vitro ... ...

Abstract	Loss of glutamatergic synapses is thought to be a key cellular pathology associated with neuropsychiatric disorders including schizophrenia (SCZ) and major depressive disorder (MDD). Genetic and cellular studies of SCZ and MDD using in vivo and in vitro systems have supported a key role for dysfunction of excitatory synapses in the pathophysiology of these disorders. Recent clinical studies have demonstrated that the estrogen, 17β-estradiol can ameliorate many of the symptoms experienced by patients. Yet, to date, our understanding of how 17β-estradiol exerted these beneficial effects is limited. In this study, we have tested the hypothesis that 17β-estradiol can restore dendritic spine number in a cellular model that recapitulates the loss of synapses associated with SCZ and MDD. Ectopic expression of wildtype, mutant or shRNA-mediated knockdown of Disrupted in Schizophrenia 1 (DISC1) reduced dendritic spine density in primary cortical neurons. Acute or chronic treatment with 17β-estradiol increased spine density to control levels in neurons with altered DISC1 levels. In addition, 17β-estradiol reduced the extent to which ectopic wildtype and mutant DISC1 aggregated. Furthermore, 17β-estradiol also caused the enrichment of synaptic proteins at synapses and increased the number of dendritic spines containing PSD-95 or that overlapped with the pre-synaptic marker bassoon. Taken together, our data indicates that estrogens can restore lost excitatory synapses caused by altered DISC1 expression, potentially through the trafficking of DISC1 and its interacting partners. These data highlight the possibility that estrogens exert their beneficial effects in SCZ and MDD in part by modulating dendritic spine number.
MeSH term(s)	Dendritic Spines ; Depressive Disorder, Major ; Estradiol/pharmacology ; Estrogens ; Humans ; Synapses
Chemical Substances	Estrogens ; Estradiol (4TI98Z838E)
Language	English
Publishing date	2020-01-21
Publishing country	United States
Document type	Journal Article ; Research Support, N.I.H., Extramural ; Research Support, Non-U.S. Gov't
ZDB-ID	2609311-X
ISSN	2158-3188 ; 2158-3188
ISSN (online)	2158-3188
ISSN	2158-3188
DOI	10.1038/s41398-020-0682-4
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