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A research team led by the University of California, Irvine has linked the mutation that causes Huntington’s disease to developmental deficits in the brain’s oligodendrocyte cells that are caused by changes in metabolism. They found that high doses of thiamine and biotin can restore normal processes.
OL cells generate the insulating coating around neurons, called myelin. The study, published online in the journal Nature Communications, provides detailed insight into the entire process of how these changes in the genes that regulate cell metabolism impair development of OLs, as well as the therapeutic value of treating HD with high doses of thiamine and biotin. Thiamine and biotin are both B vitamins and are involved in a wide range of metabolic processes that help keep the nervous system healthy.
“Our findings validate that the mutation that causes HD leads to maturation deficits in the myelin-producing cells and show that high-dose thiamine and biotin treatment restores normal function of those cells,” said Leslie Thompson, Ph.D., co-corresponding author and Donald Bren and Chancellor’s professor in the departments of psychiatry & human behavior and biological chemistry at the UCI School of Medicine, and neurobiology & behavior in the School of Biological Sciences.
Using advanced modeling methods, researchers confirmed that in mouse and human HD brain tissue, the maturation state of OL cells and their precursors are arrested in intermediate development, impairing production of the myelin that is critical for neuronal health and function. They found that high doses of thiamine and biotin were connected to significant rescue of gene expression changes in OL cells.
“The mechanisms of HD OL pathology and how these changes occur haven’t been fully understood,” said Ryan Lim, Ph.D., study co-first author and MIND Research Unit project scientist. “Our next steps will be to longitudinally track the effects of thiamine and biotin treatment on HD mice, so that we can further clarify those molecular and cellular processes, assess the efficacy of this therapeutic approach and identify other targets that may benefit HD patients.”
Team members also included co-corresponding author Dr. James E. Goldman, professor of pathology & cell biology, Columbia University College of Physicians & Surgeons; and co-first authors Jie Wu, project scientist at the UCI School of Medicine; and Osama Al Dalahmah, assistant professor of pathology& cell biology, Columbia University College of Physicians & Surgeons; as well faculty and graduate students from the Massachusetts Institute of Technology; and the City University of New York.
This work was funded, in part, by the National Institutes of Health under award numbers R35 NS116872, P01 NS092525 and R01 NS08907.
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A perplexing range of neurodegenerative diseases are known to attack distinct regions of the brain, causing severe cognitive and motor deficit. The combined impact of these (generally fatal) diseases has inflicted a devastating toll on society. New insights suggest many of these afflictions have their origin in a constellation of common processes, which play out in different ways as each disease develops.
In a study appearing in the current issue of Alzheimer’s & Dementia: The Journal of the Alzheimer’ Association, corresponding author Carol Huseby of Arizona State University and her colleagues look at cellular alterations in six distinct neurodegenerative diseases: amyotrophic lateral sclerosis or Lou Gehrig’s disease, Alzheimer’s disease, Friedreich’s ataxia, frontotemporal dementia, Huntington’s disease and Parkinson’s disease.Carol Huseby is a researcher with the ASU-Banner Neurodegenerative Disease Research Center.
The study uses an innovative approach, which includes the machine learning analysis of RNA found in whole blood. By comparing multiple diseases, researchers can identify which RNA markers occur across several neurodegenerative diseases and which are unique to each disease.
“It appears that multiple neurodegenerative diseases harbor similar fundamental dysfunctional cellular processes,” says Huseby, a researcher with the ASU-Banner Neurodegenerative Disease Research Center. “Differences between diseases may be key to discovering regional cell-type vulnerabilities and therapeutic targets for each disease.”
The blood samples used for the study were derived from a publicly available data set known as the Gene Expression Omnibus. Each of the six neurodegenerative diseases were probed. As the machine learning algorithm combed through thousands of genes, it assembled sets of RNA transcripts that optimally classified each disease, comparing the data with RNA samples from healthy patient blood.
The selected RNA transcripts reveal eight common themes across the six neurodegenerative diseases: transcription regulation, degranulation (a process involved in inflammation), immune response, protein synthesis, cell death or apoptosis, cytoskeletal components, ubiquitylation/proteasome (involved in protein degradation) and mitochondrial complexes (which oversee energy usage in cells). The eight cellular dysfunctions uncovered are associated with identifiable pathologies in the brain characteristic of each disease.

Nerve cells need a lot of energy and oxygen. They receive both through the blood. This is why nerve tissue is usually crisscrossed by a large number of blood vessels. But what prevents neurons and vascular cells from getting in each other’s way as they grow? Researchers at the Universities of Heidelberg and Bonn, together with international partners, have identified a mechanism that takes care of this. The results have now appeared in the journal Neuron.
Nerve cells are extremely hungry. About one in five calories that we consume through food goes to our brain. This is because generating voltage pulses (the action potentials) and transmitting them between neurons is very energy-intensive. For this reason, nerve tissue is usually crisscrossed by numerous blood vessels. They ensure a supply of nutrients and oxygen.
During embryonic development, a large number of vessels sprout in the brain and spinal cord, but also in the retina of the eye. Additionally, masses of neurons are formed there, which network with each other and with structures such as muscles and organs. Both processes have to be considerate of each other so as not to get in each other’s way. “We have identified a new mechanism that ensures this,” explains Prof. Dr. Carmen Ruiz de Almodóvar, member of the Cluster of Excellence ImmunoSensation2 and the Transdisciplinary Research Area Life & Health at the University of Bonn.
The researcher moved to the Institute of Neurovascular Cell Biology at the University Hospital Bonn in early 2022. Since this spring, she has held one of the special established Schlegel Professorships, with which the university aims to attract outstanding researchers to Bonn. However, most of the research was still done at her old place of work, the European Center for Angioscience at the Medical Faculty Mannheim, which is part of the University of Heidelberg. The work was then completed at the University of Bonn. In her study, she and international partners took a close look at the formation of blood vessels in the spinal cord of mice.
Growth pause in the spine
“The appearance of blood vessels in the spinal cord begins in the animals about 8.5 days after fertilization,” she says. “Between days 10.5 and 12.5, however, blood vessels do not grow in all directions. This is despite the fact that large amounts of growth-promoting molecules are present in their environment during this time. Instead, during this time, numerous nerve cells — the motor neurons — migrate from their place of origin in the spinal cord to their final position. There, they then form extensions called axons that lead from the spine to the various targeting muscles.”
This means that the motor neurons self-organize and grow at the time that blood vessels do not grow towards them. Only then after, do the vessels begin to sprout again. “The whole thing resembles a carefully choreographed dance,” explains José Ricardo Vieira. The doctoral student in Ruiz de Almodóvar’s research group did much of the work in the study. “In the course of this, each partner takes care not to get in the other’s way.”

Dystonias are potentially disabling neurological conditions that can greatly affect quality of life. Effective treatments are sparse, with botulinum toxin (Botox) injections into the affected muscles considered the first-line therapy. However, the injections do not work for every patient with dystonia, and there has been no established way for clinicians to determine who would benefit and who would not prior to treatment initiation.
In a new study published November 28 in Annals of Neurology, an artificial intelligence platform called DystoniaBoTXNet used brain MRIs to automatically identify which patients would respond to botulinum toxin treatment with 96.3 percent accuracy. Such a platform can inform clinicians’ treatment decisions, according to senior study author Kristina Simonyan, MD, PhD, Dr med, director of Laryngology Research at Mass Eye and Ear, a member of Mass General Brigham, and professor of Otolaryngology-Head and Neck Surgery at Harvard Medical School.
“Typically, a patient with dystonia would undergo a series of dose- and location-finding injections to determine whether botulinum toxin relieves their symptoms. Injections are painful and costly,” said Dr. Simonyan. “Yet, some may find no benefits from this treatment despite multiple injection attempts, while some might benefit from injections but give up after only one dose or forgo the treatment altogether. With this artificial intelligence algorithm, we can empower clinicians and patients in their therapeutic decision-making by providing them with an objective tool to replace the trial-and-error approach to botulinum toxin efficacy.”
Pervasive Treatment Challenges for Patients with Dystonia
People with dystonias experience involuntary contractions or tensing of muscles which can lead to uncontrolled movements that significantly impact physical and emotional quality of life. Isolated focal dystonias affect one part of the body, with common examples including: laryngeal dystonia affecting the vocal cords when speaking, blepharospasm causing involuntary eyelid twitching, cervical dystonia causing the neck muscles to contract and the head to twist painfully and writer’s cramp dystonia affecting the fingers during writing. About 35 of every 100,000 people have isolated or primary dystonia — a prevalence that is likely underestimated due to challenges diagnosing the disorder.
Botulinum toxin injections are considered the first-line treatment for focal dystonias. The injection paralyzes the affected muscle, aiming to prevent the involuntary contractions. The effects are usually temporary, and an injection often needs to be repeated every three-four months for life.

Middle-aged smokers are far more likely to report having memory loss and confusion than nonsmokers, and the likelihood of cognitive decline is lower for those who have quit, even recently, a new study has found.
The research from The Ohio State University is the first to examine the relationship between smoking and cognitive decline using a one-question self-assessment asking people if they’ve experienced worsening or more frequent memory loss and/or confusion.
The findings build on previous research that established relationships between smoking and Alzheimer’s Disease and other forms of dementia, and could point to an opportunity to identify signs of trouble earlier in life, said Jenna Rajczyk, lead author of the study, which appears in the Journal of Alzheimer’s Disease.
It’s also one more piece of evidence that quitting smoking is good not just for respiratory and cardiovascular reasons — but to preserve neurological health, said Rajczyk, a PhD student in Ohio State’s College of Public Health, and senior author Jeffrey Wing, assistant professor of epidemiology.
“The association we saw was most significant in the 45-59 age group, suggesting that quitting at that stage of life may have a benefit for cognitive health,” Wing said. A similar difference wasn’t found in the oldest group in the study, which could mean that quitting earlier affords people greater benefits, he said.
Data for the study came from the national 2019 Behavioral Risk Factor Surveillance System
Survey and allowed the research team to compare subjective cognitive decline (SCD) measures for current smokers, recent former smokers, and those who had quit years earlier. The analysis included 136,018 people 45 and older, and about 11% reported SCD.

A new study from researchers at Uppsala University presents novel findings on why human lymph nodes lose their function with age and the consequences for the effectiveness of our immune system. The article has been published in The Journal of Pathology.
Lymph nodes normally serve as the headquarters of our immune system. When we get an infection or are vaccinated, the lymph nodes are the sites where the immune cells congregate, are activated and proliferate so as to be able to mobilise an effective immune defence. However, as we age, the normal tissue in the lymph nodes (the stroma) is gradually replaced by adipose tissue (fat). The phenomenon is known as lymph node lipomatosis. Although lipomatosis is very common and increases with age, researchers have previously devoted very little discussion and research to it.
By careful analysis of more than 200 lymph nodes, Maria Ulvmar’s group demonstrates that lipomatosis begins in the central part of the lymph node, known as the medulla, and presents evidence linking lipomatosis to the transformation of the supporting cells of lymph nodes (fibroblasts) into adipocytes (fat cells). They also show that specific types of fibroblasts located in the medulla are more prone to become adipocytes.
The study shows that even at early stages of lipomatosis, negative changes arise that impair the ability of the lymph node to provide effective immunity. Among other observations, they note that the specialised blood and lymphatic vessels that normally provide channels for immune cells to enter and leave the lymph node are destroyed in the parts of the node where fat has formed. Lipomatosis of lymph nodes, even at early stages, may therefore be one important factor behind the poorer response to vaccinations observed in elderly people. Ultimately, the fat completely takes over the lymph node and it loses its ability to function.
“Our study is a first step towards understanding why lipomatosis occur, and towards the longer term goal of finding ways to prevent its progression and the destruction of the lymph node,” says Tove Bekkhus, first author of the study.
The researchers are currently unable to mimic the effects they observe in human lymph nodes in the animal models that are often used to study the effects of ageing. This underlines the importance of studies based on direct analysis in human subjects of the changes associated with ageing.
“I hope our work will spur an interest among other researchers in including lymph nodes lipomatosis as a factor when studying elderly people’s responses to vaccination and infections. The changes we observe are also highly relevant to cancer research, since in several types of cancer, the lymph nodes are the first place cancer cells spread to,” explains Maria H. Ulvmar, researcher at Uppsala University, who led the study.
“Our publication provides the first chapter of a story about fat and loss of function in our lymph nodes when we age. We will now continue to develop this story by designing new studies to learn more about the underlying causes and consequences of these changes,” Ulvmar says.
The main material analysed in the study consists of biobank samples from Uppsala Biobank. These samples have been analysed using advanced image analysis. The study also includes analysis and experiments using cell cultures from primary stromal cells and bioinformatic analysis of gene expressions (RNA level) from two single cell RNA sequencing (RNAseq) data sets, mouse and human, previously published by others but now analysed in this study to find answers to new specific questions.
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Researchers from Children’s Hospital of Philadelphia (CHOP) and New Jersey Institute of Technology (NJIT) developed new software that integrates a variety of information from a single cell, allowing researchers to see how one change in a cell can lead to several others and providing important clues for pinpointing the exact causes of genetic-based diseases.
The findings were published by Nature Communications.
Single-cell sequencing allows researchers to look at specific aspects of a cell to determine how it interacts with its microenvironment. This is particularly relevant in cancer research since it can be used to determine the effects of a mutation that may only affect a small portion of cells. At the single-cell level, researchers can study gene expression as well as messenger RNA, proteins and even organelles within the cells in much greater detail and resolution than before.
However, because each of the characteristics of a single cell has been studied individually, their connections with one another — for example, how a genetic variant might directly impact messenger RNA, protein synthesis or epigenetics — may not be apparent, even when comparing data generated from the same cell.
To address this statistical and computational dilemma, the researchers developed an automated single-cell multimodal sequencing clustering software tool to profile what is happening within the cell across multiple biological processes simultaneously and better characterize relationships between changes in a cell.
“With this tool, we can better understand a single cell as an entity and not just as a fragmented unit,” said Hakon Hakonarson, MD, PhD, director of the Center for Applied Genomics at CHOP and a senior author of the study. “This is a significant advancement and allows us to integrate and put all of this information into biological perspective, which is particularly important when considering information on different diseases.”
The software, referred to as single-cell multimodal deep clustering (scMDC), uses machine learning to analyze data about different characteristics of a single cell. The researchers conducted extensive simulation and real-data experiments and found that scMDC outperformed existing single cell single-modal and multimodal clustering methods on single-cell multimodal data sets. It also utilizes linear scalability, meaning that more data sources provided to the scMDC yield better results.
This study was supported by National Institutes of Health grant R15HG012087 and the National Center for Advancing Translational Sciences under grant number UL1TR003017. The computing resource was partially provided by Extreme Science and Engineering Discovery Environment (XSEDE) through allocation CIE160021 and CIE17003, supported by National Science Foundation Grant ACI-1548562.
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The brain cancer, glioblastoma, is a fierce and formidable opponent. Its millions of victims include Senator John McCain, President Biden’s son, Beau, and famed film critic Gene Siskel, to name just a few. Most patients succumb within two years and few make it past five, a statistic that hasn’t improved in decades due to lack of effective treatment options.
“The aggressiveness of glioblastoma is notorious,” says Cold Spring Harbor Laboratory (CSHL) Professor Alea Mills. “The norm is to do surgery, treat with harsh drugs, and just hope for the best.” But now, Mills and her colleagues have discovered in this deadly cancer a vulnerability, known as BRD8, that may finally lead to new treatment options and better patient outcomes.
The CSHL team recently solved a decades-old mystery surrounding glioblastoma’s aggressiveness by linking the BRD8 protein to another protein, named P53. A staple in the body’s natural cancer defenses, P53 prevents cells from overgrowing and turning into tumors. Almost all cancers depend on P53 becoming mutated and thus disabled. But weirdly, in the majority of glioblastoma cases, P53 is unscathed. “So why does this cancer act like P53 is broken?” asked CSHL postdoctoral fellow Xueqin Sun. This critical question led Mills’ team to discover that BRD8 had gone rogue in glioblastoma, crippling P53 in a completely new way.
BRD8 shuts down access to genes in chromosomes. If a gene is wound up tightly, it cannot be used — it’s as if it were “asleep.” Mills and her team revealed that BRD8 was inappropriately active in glioblastoma, keeping many of P53’s critical anticancer defenses at rest. When the researchers inactivated BRD8 via genome editing, P53’s “arsenal” suddenly woke up and began blocking tumor growth.
“It’s like BRD8 is saying ‘NO ENTRY’ to P53’s tumor-preventing power, but when we hit BRD8 in the right way — go in there almost like a scalpel, but molecularly — the tumor is annihilated,” Mills explains. She and her team implanted tumor cells from glioblastoma patients into mice and watched the tumors grow in the brain. When BRD8 was inactivated, P53 was unlocked — the tumors stopped growing and the mice lived longer.
The finding suggests that drugs targeting the heart of BRD8 could work against glioblastoma. Mills hopes her team’s discovery will help turn this deadly brain cancer into a treatable disease and for the first time in a generation, extend the life expectancy of patients who are diagnosed with it.
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Materials provided by Cold Spring Harbor Laboratory. Original written by Luis Sandoval. Note: Content may be edited for style and length.

Researchers at the Sainsbury Wellcome Centre and Gatsby Computational Neuroscience Unit at UCL have revealed a brain mechanism that mice use to instinctively escape to shelter when faced with a threat. This is the first time that neuroscientists have been able to find such a clear link between spatial goals and actions.
The study, published today in Nature, explains how mice incorporate knowledge of safe locations to execute the most efficient route to shelter. The neuroscientists found that two areas of the mouse brain, the retrosplenial cortex (RSP) and superior colliculus (SC), form a circuit that encodes the direction to a shelter. When faced with a threat, the RSP-SC circuit enables mice to accurately orient to shelter and escape to safety.
“If a fire alarm sounded right now, you would instinctively know how to leave the room to get to safety. This is because your brain continuously keeps track of where the exit is at all times. This happens unconsciously, you don’t have to think about it. We wanted to understand how the brain uses such important spatial information to navigate to a goal location as quickly as possible,” said Professor Tiago Branco, Group Leader at the Sainsbury Wellcome Centre and corresponding author on the paper.
From previous studies, it was known that this process is memory-based. Some people that have lesions in the RSP are still able to remember familiar locations, but they are disoriented in space and lose the ability to connect an action to a spatial goal. For example, they might know where the door is but they don’t know what actions to take to get there.
To help understand how the brain uses spatial memories to guide actions, the Branco lab used miniature electrodes, called Neuropixels probes, to simultaneously record from two regions of the mouse brain — the RSP and SC — as they were presented with a threatening sound.
“We found that the RSP is computing shelter direction and then sending this information to the SC, which uses this direction to turn the mouse’s head. When we perturbed the connection between these two regions, preventing the RSP talking to the SC, the mouse ran in a random direction when scared. This tells us that the RSP-SC circuit is a critical pathway for knowing where the shelter is and orienting to it,” explained Professor Branco.
“At a cellular level, the connection between RSP and SC is wired up in an intelligent manner that allows it to exploit the local organisation of inhibitory and excitatory SC neurons to inject the shelter memory into the SC. The result is that cortical cells generate a localised bump of activity on the SC network that is much like the needle of a compass, continuously pointing to the shelter as the mouse explores the environment. Similar circuit motifs have been observed in various organisms, from flies to fishes, perhaps suggesting a conserved blueprint for mapping direction across the animal kingdom,” commented Dr Dario Campagner, Research Fellow at the Sainsbury Wellcome Centre and Gatsby Computational Neuroscience Unit and joint first author on the paper
To further test this finding, the neuroscientists included a second identical shelter but with a closed entrance. They found that the RSP represents both the closed and the open shelter, but the SC represents only the open one. One possible explanation is that the RSP represents lots of possible goals and the SC selects the one that is most important for the particular context, in this case the open shelter that confers safety.
“Our work shows how a rapid instinctive behaviour as anti-predatory escape can be endowed with flexibility. While the drive to escape is innate, the implementation of escape relies on a cortical spatial memory signal arriving in the SC to inform where the goal location lies. This signal maps the shelter location in egocentric space, a readily usable information format for the SC, allowing rapid implementation of orientation to shelter,” said Dr Ruben Vale, joint first author on the paper.
The next question for the researchers is to understand how the brain continuously updates important spatial information. The team hypothesise that this involves the combination of sensory and self-motion cues, such as vestibular information. To explore this further, neuroscientists in the Branco and Margrie labs at SWC are doing comparative studies in other species including Fiddler crabs that exhibit the same escape behaviour as mice but have a simpler nervous system. This will allow the researchers to look for shared principles of how the different species solve this very important problem.
This research was funded by a Wellcome Senior Research Fellowship (214352/Z/18/Z) and by the Sainsbury Wellcome Centre Core Grant from the Gatsby Charitable Foundation and Wellcome (090843/F/09/Z), MRC PhD Studentship, Boehringer Ingelheim Fonds PhD fellowship, Gatsby Unit/SWC Joint Research Fellowship in Neuroscience, UCL Wellcome 4-year PhD Programme in Neuroscience, A*STAR National Science Scholarship and the SWC PhD Programme.

Researchers at the Universitat Pompeu Fabra (UPF), ICREA, CIBERNED, CNIC and Altos Labs, among other national and international collaborators, have characterized how damaged cells (senescent cells) that inevitably arise after injury negatively impact tissue regeneration, and how this mechanism operates actively in old age, but surprisingly also in young age. This negative action can be overcome genetically and pharmacologically, hence restoring stem cell regenerative functions.
Tissue regeneration depends on a population of stem cells and its neighbouring cells, a process whose efficacy declines with aging. The reasons of this decline remain largely unknown.
Dr. Pura Muñoz-Cánoves, ICREA professor at the Department of Medicine and Life Sciences (MELIS) at UPF in Barcelona, CNIC in Madrid, and CIBERNED, and now in Altos Labs San Diego Institute of Science, and Dr. Eusebio Perdiguero (also from MELIS and now in Altos Labs), have found in experiments with mice that senescent cells are new regulatory components of the muscle tissue regenerating niche that blunt muscle regeneration at all stages of life.
Cellular senescence is a state of irreversible cell cycle arrest that often emerges after tissue damage and in age-related diseases. Cells don’t die but remain in a hibernation state. Together with apoptosis (a form of programmed cell death), senescence is one of the mechanisms the body uses to control the unwanted proliferation shown by tumours. Therefore, the study of these cells is of great biomedical relevance. In addition, senescent cells affect tissue repair processes, and beneficial effects as tumour suppressors have been documented during embryo development and in liver and skin repair or reprogramming.
Despite these reasons, few studies had attempted to profile and characterize them in vivo. This is largely attributed to the rarity and scarcity of these cells, even in aged tissues.
In a study published today in Nature, the team of researchers generated the first transcriptomic atlas of senescent cells of damaged skeletal muscle of mice of distinct ages (transcriptomic refers to everything related to RNA or the structures that transcript the information encoded originally inside a nucleus cell). Researchers found that senescent cells are widely heterogeneous, yet they display common traits, including the secretion of proinflammatory and profibrotic (that promotes an excess of fibrous connective tissue) factors. This secretion in turn, impacts the nearby stem cells and hampers their regenerative capacity, thus impairing muscle regeneration. So, it appears that what once was as a good protection tool now turns into a bad one.
Results showed that reducing the load of senescent cells (either through genetic or pharmacological treatments that induce death of these cells) improved the regeneration of aged muscles and, unexpectedly also, of young muscle. These benefits in young tissue are due to reduction of inflammation in the stem cell nearby environment, which fosters stem cell functions.
“This is consistent with the notion that senescent cells, even in young tissues, create a hyper inflamed microenvironment that mirrors inflammation associated to ageing (inflammaging),” says Pura Muñoz-Cánoves. Thus, senescent cells provoke the anticipated ageing of the stem cell niche even in young mice; hence, reducing the senescent burden, attenuates inflammation of the stem cell niche and improves muscle repair.
“In addition to the biomedical benefits of targeting senescent cells, the new molecular information provided by the muscle senescent cell atlas could be likely transferred to understanding the function of senescence in other tissues whose senescent cells have either not been profiled at all or lack enough senescent cell numbers,” says Dr. Eusebio Perdiguero.
Increasing work from many groups demonstrates that the effects of senescent cells are diverse (beneficial or detrimental) and depend on the tissue environment and type, the duration of injury, the degree of persistence of senescent cells, and the organism’s age. Thus, “the roles of senescent cells should be studied in distinct contexts, in normal, aged and disease states,” indicates Dr. Muñoz-Cánoves. In this line, she adds that “altogether, the information shown in this paper will be instrumental for advancing our knowledge of senescent cells and finding new treatments to target them in the context of regenerative medicine and aging.”
This scientific study has also involved the collaboration of researchers at the Kyushu University, (Fukuoka, Japan), Altos Labs San Diego Institute (San Diego, USA), University of Tokyo (Tokyo, Japan), Guangzhou Institutes of Biomedicine and Health, Chinese Academy of Sciences (Guangzhou, China), CIC bioGUNE (Derio, Spain), Institute for Research in Biomedicine (IRB Barcelona), Luxembourg Centre for Systems Biomedicine (LCSB), University of Luxembourg (Luxembourg). The study was funded in part by grants from the European Research Council (ERC), the Spanish Ministry of Science and Innovation, La Caixa Foundation, AFM, MDA, MWRF, and DPP-Spain.