PEOPLEAndrew Hicks

de en it

Andrew Hicks

Vice Head of Institute
Institute for Biomedicine

T +39 0471 055 521

andrew.hicks@eurac.edu

https://orcid.org/0000-0001-6320-0411

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About

Main Research Interests

Being Vice Head of the Institute for Biomedicine involves interacting with the senior management team of the Institute to develop and execute the strategic development of the Institute overall, in order to help achieve our mission and vision. As Group Leader of the Translational Biology programs at the Institute, my main focus is to map the genes involved in complex diseases of the population, study the interactions between these gene and environment, and look for opportunities to develop specific targets towards products and services and solutions that can positively impact the health of the population. Currently we have active research programs to identify functionality of genes associating with Parkinson’s disease, and whether these can be manipulated for potential therapeutic benefit using novel biological drugs. We are also working on genetic targets for Arrhythmogenic Crdiomyopathy and are establishing research programs into mechanisms of neuronal hyperexcitability that might underlie chronic pain and neurodevelopmental disorders and epilepsy. We are trying to orient our research not only to basic cellular mechanisms with the goal of identifying pathways and targets that could lead to new opportunities for potential intervention, but are focussed on taking initial steps to develop novel interventional strategies within a precision health approach.

Short C.V.

From 1981-1985 I studied Biochemistry (with supplemental Chemical Pharmacology) at Oxford University (LMH) in what is now the MBiochem. program, obtaining my Bachelors (B.A.) and Masters (M.A.) degrees. From there I moved to Cambridge (Pembroke), and from 1985-1989 obtained my PhD at the MRC Molecular Neurobiology unit on the site of the Laboratory of Molecular Biology (LMB). During this time (1988) I also spent 6 months at the NIH laboratory of Dr J.C. Venter. From 1989-1992 I stayed in Cambridge as a Senior Research Associate for Neuroscience at Peterhouse, studying neurotransmitter receptor genes as candidates in neurological and psychiatric disorders. I then moved to France, and from 1992-1998 was a Project Director in the CNRS laboratory of Jacques Mallet, investigating changes of gene expression in models of synaptic plasticity. I then moved to Iceland (via the Faroe Islands) and from 1998-2007 was the Project Leader and Director of Movement Disorder Genetics within the CNS division of deCODE genetics Inc. with a focus on the genetics of Parkinson’s disease and Restless legs Syndrome. During this time (1998-2003) I acted as a part-time consultant to the Government of the Faroe Islands to help in establishing the framework for genetic research on the Islands. In 2007 I moved to what is now the Institute for Biomedicine at Eurac Research, holding positions of Deputy Scientific Director and Group Leader for Molecular Medicine and then Neuromedicine groups. Since 2018 my role is Vice Head of Institute and Group Leader for Translational Genomics, which in 2024 became Translational Biology overall, by merging the Translational Genomics and Translational Human Models groups. Overall, I have been working for the last 25 years in the field of complex disease genetics, both mapping genes and establishing functional research programs with experimental human cell models to investigate the role of genes in disease mechanisms, and look for potential points of intervention with novel biological drugs .

Google Scholar: https://scholar.google.com/citations?user=2lcHjOsAAAAJ&hl=en

ORCID: https://orcid.org/0000-0001-6320-0411

LinkedIn: https://www.linkedin.com/in/andrew-hicks-86032a/

Research Gate: https://www.researchgate.net/profile/Andrew-Hicks-5

Twitter: @andrewhicks

Scientific Publications

Journal article2025

Large-scale copy number variant analysis in genes linked to Parkinson´s disease.

Landoulsi Z, Lohmann K, Vollstedt EJ, Wedgwood-Benn E, Niestroj LM, Laabs BH, Sendel S, Balck A,

Andrew Hicks, Peter P. Pramstaller

Genetic studies of Parkinson's disease (PD) have focused on single nucleotide variants (SNVs), with limited attention to copy number variants (CNVs). This study investigates CNVs in PD using candidate PD-related genes and genome-wide approaches. We identified CNVs from the ProtectMove project genotyping data of 2364 PD patients and 2909 controls using PennCNV. We validated 119 of 137 detected CNVs in PD-related genes (87%) using MLPA/qPCR, including 104 in PRKN, six in PARK7, four in SNCA, and others in LRRK2, RAB32, and VPS35. CNVs were present in 2.4% of patients and 1.5% of controls. Notably, 0.9% of patients carried potentially disease-causing CNVs compared to 0.1% in controls. CNVs were enriched in patients (OR = 1.67, p = 0.03) due to PRKN CNVs, particularly in early-onset cases. These results highlight the importance of CNVs in PD, particularly in PRKN, and suggest that rare CNVs in LRRK2 and RAB32 may contribute to disease risk and diagnostic potential.

DOI

DOI: 10.1038/s41531-025-01076-y

Journal article2025

Protocol for recording of neural activity in 3D midbrain organoids using a multiple-electrode array

Malkoc A, Riekschnitz D, Rosato Siri M, Hicks A, Pramstaller P, Pischedda F, Volta M

Andrew Hicks, Mattia Volta, Peter P. Pramstaller, Diana Riekschnitz, Marcelo Rosato Siri

Project: The molecular biology of Neurocovid

Here, we present a protocol for electrophysiological recording from human three-dimensional (3D) organoids using substrates designed for two-dimensional cultures. We describe steps for generating midbrain 3D organoids from human induced pluripotent stem cells (hiPSCs) utilizing 6-well multi-electrode array (MEA) plates. We then detail procedures for recording neuronal activity via the neural module for Axion Maestro system. Our approach provides neural recording in organoids with high reliability and reproducibility, opening new avenues for research into human neurodevelopment and disease modeling.

DOI

DOI: 10.1016/j.xpro.2025.104208

Journal article2025

The influence of affective temperaments on sleep quality in a general population sample. Data report from the CHRIS study

Favaretto E, Gögele M, Bedani F, Giovannini S, Pramstaller PP, Perugi G, Erfurth A, Sani G,

Andrew Hicks, Martin Gögele, Roberto Melotti, Peter P. Pramstaller

Background: Affective temperaments predispose to life adaptation and affective disorders. The relationship between temperaments and sleep quality is rarely investigated in community-based studies. We hypothesized that cyclothymic-related temperaments relate to worse sleep quality, whereas the hyperthymic temperament favours sleep quality.

Method: We investigated 3701 18 to 65 years old adults from the population-based CHRIS study in Italy. Participants were 54 % females, mean age 38.5 years. The Pittsburgh Sleep Quality Index (PSQI) was the primary outcome score. Five affective temperaments split into quartiles for direct comparison from the TEMPS-M questionnaire were the exposures of interest. Additional covariates comprised sex, age, trait anxiety, and sleep quality-related lifestyles assessed via interviews, self-administered questionnaires or instrumental measurements.

Results: The hyperthymic temperament showed a negative association (better sleep quality) with the global PSQI, whereas the cyclothymic-related temperaments had all associations in opposite direction. While inclusion of trait anxiety appeared to mediate some results, the anxious and other cyclothymic related temperaments were still directly associated with multiple dimensions of poor sleep quality.

Limitations: The cross-sectional design, possible selection into the study by temperamental background or sleep disorders, and no clinically validated self-assessed psychiatric constructs represent possible weaknesses.

Conclusions: Our findings support the hypothesis of a biological binary diathesis of affective temperaments, with hyperthymic and cyclothymic-related temperaments predisposing sleep quality in an antithetical way.

DOI Source

DOI: 10.1016/j.jad.2025.03.055

Journal article2024

Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits

Keaton JM, Kamali Z, Xie T, Vaez A, Williams A, Goleva SB, Ani A, Evangelou E,

Andrew Hicks

Hypertension affects more than one billion people worldwide. Here we identify 113 novel loci, reporting a total of 2,103 independent genetic signals (P < 5 × 10^-8) from the largest single-stage blood pressure (BP) genome-wide association study to date (n = 1,028,980 European individuals). These associations explain more than 60% of single nucleotide polymorphism-based BP heritability. Comparing top versus bottom deciles of polygenic risk scores (PRSs) reveals clinically meaningful differences in BP (16.9 mmHg systolic BP, 95% CI, 15.5-18.2 mmHg, P = 2.22 × 10^-126) and more than a sevenfold higher odds of hypertension risk (odds ratio, 7.33; 95% CI, 5.54-9.70; P = 4.13 × 10^-44) in an independent dataset. Adding PRS into hypertension-prediction models increased the area under the receiver operating characteristic curve (AUROC) from 0.791 (95% CI, 0.781-0.801) to 0.826 (95% CI, 0.817-0.836, ∆AUROC, 0.035, P = 1.98 × 10^-34). We compare the 2,103 loci results in non-European ancestries and show significant PRS associations in a large African-American sample. Secondary analyses implicate 500 genes previously unreported for BP. Our study highlights the role of increasingly large genomic studies for precision health research.

DOI

DOI: 10.1038/s41588-024-01714-w

Journal article2024

How to communicate and what to disclose to participants in a recall-by-genotype research approach: A multistep empirical study

Tschigg K, Consoli L, Brüggemann N, Hicks AA, Staunton C, Mascalzoni D, Biasiotto R

Andrew Hicks, Deborah Mascalzoni, Roberta Biasiotto

Recall-by-genotype (RbG) is a bottom-up approach using existing genetic data to design follow-up stratified studies. Genetic information may be partially disclosed at invitation, thus raising ethical issues which call for defined best practices for disclosure and communication in RbG approaches. Within the context of the ProtectMove sub-project of the Cooperative Health Research in South Tyrol (CHRIS) study, we investigated research participant perspectives on RbG communication strategies (Step 1 and 4, questionnaire with a subsample of CHRIS participants with and without previous experience of RbG, respectively). Additionally, we explored researchers’ and study personnel’s experience with RbG (Step 2 and 3, focus group discussion). In step 1 (N = 95), participants were generally satisfied with the study process. Most (71.6%) wanted to know their carrier status for personal and collective benefit. Tailored disclosure strategies and transparent, effective, and well-thought-out communication approaches were advocated by study personnel (Step 2, N = 6) and researchers (Step 3, N = 7). Challenges in dealing with uncertainty, concerns caused by RbG invitations, and the possibility of misunderstanding were also raised. In step 4 (N = 369), participants valued being informed of study details at the first invitation stage, and generally felt comfortable towards RbG study invitations (58.5%) and to receiving genetic information after the study (58.5–81.6%). Comfort and perceived impact of disclosure of genetic information varied according to the type of variant being potentially disclosed. This study suggested designing communication strategies, based on clear and understandable explanations, sensitive to participant expectations and preferences, developing case-by-case solutions for disclosure.

DOI Source

DOI: 10.1007/s12687-024-00733-8

Journal article2024

Hypoxia Sensing and Responses in Parkinson's Disease

Burtscher J, Duderstadt Y, Gatterer H, Burtscher M, Vozdek R, Millet GP, Hicks AA, Ehrenreich H,

Roman Vozdek, Andrew Hicks, Hannes Gatterer

Parkinson's disease (PD) is associated with various deficits in sensing and responding to reductions in oxygen availability (hypoxia). Here we summarize the evidence pointing to a central role of hypoxia in PD, discuss the relation of hypoxia and oxygen dependence with pathological hallmarks of PD, including mitochondrial dysfunction, dopaminergic vulnerability, and alpha-synuclein-related pathology, and highlight the link with cellular and systemic oxygen sensing. We describe cases suggesting that hypoxia may trigger Parkinsonian symptoms but also emphasize that the endogenous systems that protect from hypoxia can be harnessed to protect from PD. Finally, we provide examples of preclinical and clinical research substantiating this potential.

DOI

DOI: 10.3390/ijms25031759

Journal article2024

Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2

Zanon A, Guida M, Lavdas AA, Corti C, Castelo Rueda MP, Negro A, Pramstaller PP, Domingues FD,

Andrew Hicks, Irene Pichler, Alexandros Lavdas, Corrado Corti, Peter P. Pramstaller

Background: Loss-of-function mutations in the PRKN gene, encoding Parkin, are the most common cause of autosomal recessive Parkinson’s disease (PD). We have previously identified mitochondrial Stomatin-like protein 2 (SLP-2), which functions in the assembly of respiratory chain proteins, as a Parkin-binding protein. Selective knockdown of either Parkin or SLP-2 led to reduced mitochondrial and neuronal function in neuronal cells and Drosophila, where a double knockdown led to a further worsening of Parkin-deficiency phenotypes. Here, we investigated the minimal Parkin region involved in the Parkin-SLP-2 interaction and explored the ability of Parkin-fragments and peptides from this minimal region to restore mitochondrial function.

Methods: In fibroblasts, human induced pluripotent stem cell (hiPSC)-derived neurons, and neuroblastoma cells the interaction between Parkin and SLP-2 was investigated, and the Parkin domain responsible for the binding to SLP-2 was mapped. High resolution respirometry, immunofluorescence analysis and live imaging were used to analyze mitochondrial function.

Results: Using a proximity ligation assay, we quantitatively assessed the Parkin-SLP-2 interaction in skin fibroblasts and hiPSC-derived neurons. When PD-associated PRKN mutations were present, we detected a significantly reduced interaction between the two proteins. We found a preferential binding of SLP-2 to the N-terminal part of Parkin, with a highest affinity for the RING0 domain. Computational modeling based on the crystal structure of Parkin protein predicted several potential binding sites for SLP-2 within the Parkin RING0 domain. Amongst these, three binding sites were observed to overlap with natural PD-causing missense mutations, which we demonstrated interfere substantially with the binding of Parkin to SLP-2. Finally, delivery of the isolated Parkin RING0 domain and a Parkin mini-peptide, conjugated to cell-permeant and mitochondrial transporters, rescued compromised mitochondrial function in Parkin-deficient neuroblastoma cells and hiPSC-derived neurons with endogenous, disease causing PRKN mutations.

Conclusions: These findings place further emphasis on the importance of the protein-protein interaction between Parkin and SLP-2 for the maintenance of optimal mitochondrial function. The possibility of restoring an abolished binding to SLP-2 by delivering the Parkin RING0 domain or the Parkin mini-peptide involved in this specific protein-protein interaction into cells might represent a novel organelle-specific therapeutic approach for correcting mitochondrial dysfunction in Parkin-linked PD.

DOI

DOI: 10.1186/s12967-024-04850-3

Journal article2024

Nuclear and mitochondrial genetic variants associated with mitochondrial DNA copy number

Koller A, Filosi M, Weissensteiner H, Fazzini F, Gorski M, Pattaro C, Schönherr S, Forer L,

Andrew Hicks, Cristian Pattaro, Peter P. Pramstaller, Christian Fuchsberger

Mitochondrial DNA copy number (mtDNA-CN) is a biomarker for mitochondrial dysfunction associated with several diseases. Previous genome-wide association studies (GWAS) have been performed to unravel underlying mechanisms of mtDNA-CN regulation. However, the identified gene regions explain only a small fraction of mtDNA-CN variability. Most of this data has been estimated from microarrays based on various pipelines. In the present study we aimed to (1) identify genetic loci for qPCR-measured mtDNA-CN from three studies (16,130 participants) using GWAS, (2) identify potential systematic differences between our qPCR derived mtDNA-CN measurements compared to the published microarray intensity-based estimates, and (3) disentangle the nuclear from mitochondrial regulation of the mtDNA-CN phenotype. We identified two genome-wide significant autosomal loci associated with qPCR-measured mtDNA-CN: at HBS1L (rs4895440, p = 3.39 × 10^-13) and GSDMA (rs56030650, p = 4.85 × 10^-08) genes. Moreover, 113/115 of the previously published SNPs identified by microarray-based analyses were significantly equivalent with our findings. In our study, the mitochondrial genome itself contributed only marginally to mtDNA-CN regulation as we only detected a single rare mitochondrial variant associated with mtDNA-CN. Furthermore, we incorporated mitochondrial haplogroups into our analyses to explore their potential impact on mtDNA-CN. However, our findings indicate that they do not exert any significant influence on our results.

DOI

DOI: 10.1038/s41598-024-52373-0

Journal article2023

Antithrombin, Protein C, and Protein S: Genome and Transcriptome-Wide Association Studies Identify 7 Novel Loci Regulating Plasma Levels

Ji Y, Temprano-Sagrera G, Holle LA, Bebo A, Brody JA, Le NQ, Kangro K, Brown MR,

Andrew Hicks, Martin Gögele, David Emmert, Christian Fuchsberger

Background: Antithrombin, PC (protein C), and PS (protein S) are circulating natural anticoagulant proteins that regulate hemostasis and of which partial deficiencies are causes of venous thromboembolism. Previous genetic association studies involving antithrombin, PC, and PS were limited by modest sample sizes or by being restricted to candidate genes. In the setting of the Cohorts for Heart and Aging Research in Genomic Epidemiology consortium, we meta-analyzed across ancestries the results from 10 genome-wide association studies of plasma levels of antithrombin, PC, PS free, and PS total.

Methods: Study participants were of European and African ancestries, and genotype data were imputed to TOPMed, a dense multiancestry reference panel. Each of the 10 studies conducted a genome-wide association studies for each phenotype and summary results were meta-analyzed, stratified by ancestry. Analysis of antithrombin included 25 243 European ancestry and 2688 African ancestry participants, PC analysis included 16 597 European ancestry and 2688 African ancestry participants, PSF and PST analysis included 4113 and 6409 European ancestry participants. We also conducted transcriptome-wide association analyses and multiphenotype analysis to discover additional associations. Novel genome-wide association studies and transcriptome-wide association analyses findings were validated by in vitro functional experiments. Mendelian randomization was performed to assess the causal relationship between these proteins and cardiovascular outcomes.

Results: Genome-wide association studies meta-analyses identified 4 newly associated loci: 3 with antithrombin levels (GCKR, BAZ1B, and HP-TXNL4B) and 1 with PS levels (ORM1-ORM2). transcriptome-wide association analyses identified 3 newly associated genes: 1 with antithrombin level (FCGRT), 1 with PC (GOLM2), and 1 with PS (MYL7). In addition, we replicated 7 independent loci reported in previous studies. Functional experiments provided evidence for the involvement of GCKR, SNX17, and HP genes in antithrombin regulation.

Conclusions: The use of larger sample sizes, diverse populations, and a denser imputation reference panel allowed the detection of 7 novel genomic loci associated with plasma antithrombin, PC, and PS levels.

DOI Source

DOI: 10.1161/ATVBAHA.122.318213

Journal article2023

Genetic insights into resting heart rate and its role in cardiovascular disease

van de Vegte YJ, Eppinga RN, van der Ende MY, Hagemeijer YP, Mahendran Y, Salfati E, Smith AV, Tan VY,

Andrew Hicks, Luisa Foco

Resting heart rate is associated with cardiovascular diseases and mortality in observational and Mendelian randomization studies. The aims of this study are to extend the number of resting heart rate associated genetic variants and to obtain further insights in resting heart rate biology and its clinical consequences. A genome-wide meta-analysis of 100 studies in up to 835,465 individuals reveals 493 independent genetic variants in 352 loci, including 68 genetic variants outside previously identified resting heart rate associated loci. We prioritize 670 genes and in silico annotations point to their enrichment in cardiomyocytes and provide insights in their ECG signature. Two-sample Mendelian randomization analyses indicate that higher genetically predicted resting heart rate increases risk of dilated cardiomyopathy, but decreases risk of developing atrial fibrillation, ischemic stroke, and cardio-embolic stroke. We do not find evidence for a linear or non-linear genetic association between resting heart rate and all-cause mortality in contrast to our previous Mendelian randomization study. Systematic alteration of key differences between the current and previous Mendelian randomization study indicates that the most likely cause of the discrepancy between these studies arises from false positive findings in previous one-sample MR analyses caused by weak-instrument bias at lower P-value thresholds. The results extend our understanding of resting heart rate biology and give additional insights in its role in cardiovascular disease development.

DOI Source

DOI: 10.1038/s41467-023-39521-2

Journal article2023

Molecular phenotypes of mitochondrial dysfunction in clinically non-manifesting heterozygous PRKN variant carriers

Castelo Rueda MP, Zanon A, Gilmozzi V, Lavdas AA, Raftopoulou AA, Delcambre S, Del Greco M F, Klein C,

Andrew Hicks, Irene Pichler, Alexandros Lavdas, Peter P. Pramstaller

Project: Identifying Parkinson’s disease penetrance-modifying factors in the population-based Cooperative Health Research in South Tyrol (CHRIS) cohort

Homozygous or compound heterozygous (biallelic) variants in PRKN are causal for PD with highly penetrant symptom expression, while the much more common heterozygous variants may predispose to PD with highly reduced penetrance, through altered mitochondrial function. In the presence of pathogenic heterozygous variants, it is therefore important to test for mitochondrial alteration in cells derived from variant carriers to establish potential presymptomatic molecular markers. We generated lymphoblasts (LCLs) and human induced pluripotent stem cell (hiPSC)-derived neurons from non-manifesting heterozygous PRKN variant carriers and tested them for mitochondrial functionality. In LCLs, we detected hyperactive mitochondrial respiration, and, although milder compared to a biallelic PRKN-PD patient, hiPSC-derived neurons of non-manifesting heterozygous variant carriers also displayed several phenotypes of altered mitochondrial function. Overall, we identified molecular phenotypes that might be used to monitor heterozygous PRKN variant carriers during the prodromal phase. Such markers might also be useful to identify individuals at greater risk of eventual disease development and for testing potential mitochondrial function-based neuroprotective therapies before neurodegeneration advances.

DOI

DOI: 10.1038/s41531-023-00499-9

Journal article2023

Role of Ceramides and Sphingolipids in Parkinson's Disease

Vos M, Klein C, Hicks AA

Andrew Hicks

Sphingolipids, including the basic ceramide, are a subset of bioactive lipids that consist of many different species. Sphingolipids are indispensable for proper neuronal function, and an increasing number of studies have emerged on the complexity and importance of these lipids in (almost) all biological processes. These include regulation of mitochondrial function, autophagy, and endosomal trafficking, which are affected in Parkinson's disease (PD). PD is the second most common neurodegenerative disorder and is characterized by the loss of dopaminergic neurons. Currently, PD cannot be cured due to the lack of knowledge of the exact pathogenesis. Nonetheless, important advances have identified molecular changes in mitochondrial function, autophagy, and endosomal function. Furthermore, recent studies have identified ceramide alterations in patients suffering from PD, and in PD models, suggesting a critical interaction between sphingolipids and related cellular processes in PD. For instance, autosomal recessive forms of PD cause mitochondrial dysfunction, including energy production or mitochondrial clearance, that is directly influenced by manipulating sphingolipids. Additionally, endo-lysosomal recycling is affected by genes that cause autosomal dominant forms of the disease, such as VPS35 and SNCA. Furthermore, endo-lysosomal recycling is crucial for transporting sphingolipids to different cellular compartments where they will execute their functions. This review will discuss mitochondrial dysfunction, defects in autophagy, and abnormal endosomal activity in PD and the role sphingolipids play in these vital molecular processes.

DOI

DOI: 10.1016/j.jmb.2023.168000

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Journal article2024

Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2

Zanon A, Guida M, Lavdas AA, Corti C, Castelo Rueda MP, Negro A, Pramstaller PP, Domingues FD,

Andrew Hicks, Irene Pichler, Alexandros Lavdas, Corrado Corti, Peter P. Pramstaller

DOI

DOI: 10.1186/s12967-024-04850-3

Andrew Hicks

About

Scientific Publications

Large-scale copy number variant analysis in genes linked to Parkinson´s disease.

Protocol for recording of neural activity in 3D midbrain organoids using a multiple-electrode array

The influence of affective temperaments on sleep quality in a general population sample. Data report from the CHRIS study

Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits

How to communicate and what to disclose to participants in a recall-by-genotype research approach: A multistep empirical study

Hypoxia Sensing and Responses in Parkinson's Disease

Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2

Nuclear and mitochondrial genetic variants associated with mitochondrial DNA copy number

Antithrombin, Protein C, and Protein S: Genome and Transcriptome-Wide Association Studies Identify 7 Novel Loci Regulating Plasma Levels

Genetic insights into resting heart rate and its role in cardiovascular disease

Molecular phenotypes of mitochondrial dysfunction in clinically non-manifesting heterozygous PRKN variant carriers

Role of Ceramides and Sphingolipids in Parkinson's Disease

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Scientific Publications

Large-scale copy number variant analysis in genes linked to Parkinson´s disease.

Protocol for recording of neural activity in 3D midbrain organoids using a multiple-electrode array

The influence of affective temperaments on sleep quality in a general population sample. Data report from the CHRIS study

Genome-wide analysis in over 1 million individuals of European ancestry yields improved polygenic risk scores for blood pressure traits

How to communicate and what to disclose to participants in a recall-by-genotype research approach: A multistep empirical study

Hypoxia Sensing and Responses in Parkinson's Disease

Intracellular delivery of Parkin-RING0-based fragments corrects Parkin-induced mitochondrial dysfunction through interaction with SLP-2

Nuclear and mitochondrial genetic variants associated with mitochondrial DNA copy number

Antithrombin, Protein C, and Protein S: Genome and Transcriptome-Wide Association Studies Identify 7 Novel Loci Regulating Plasma Levels

Genetic insights into resting heart rate and its role in cardiovascular disease

Molecular phenotypes of mitochondrial dysfunction in clinically non-manifesting heterozygous PRKN variant carriers

Role of Ceramides and Sphingolipids in Parkinson's Disease