How fear unfolds inside our brains
Neurobiologists uncover how stress turns into fear in the brain — in conditions such as PTSD — and a method to block it
Our nervous systems are naturally wired to sense fear. Whether prompted by the eerie noises we hear alone in the dark or the approaching growl of a threatening animal, our fear response is a survival mechanism that tells us to remain alert and avoid dangerous situations.
But if fear arises in the absence of tangible threats, it can be harmful to our well-being. Those who have suffered episodes of severe or life-threatening stress can later experience intense feelings of fear, even during situations that lack a real threat. Experiencing this generalization of fear is psychologically damaging and can result in debilitating long-term mental health conditions such as post-traumatic stress disorder (PTSD).
The stress-induced mechanisms that cause our brain to produce feelings of fear in the absence of threats have been mostly a mystery. Now, neurobiologists at the University of California San Diego have identified the changes in brain biochemistry and mapped the neural circuitry that cause such a generalized fear experience. Their research, published in the journal Science on March 15, 2024, provides new insights into how fear responses could be prevented.
In their report, former UC San Diego Assistant Project Scientist Hui-quan Li, (now a senior scientist at Neurocrine Biosciences), Atkinson Family Distinguished Professor Nick Spitzer of the School of Biological Sciences and their colleagues describe the research behind their discovery of the neurotransmitters — the chemical messengers that allow the brain’s neurons to communicate with one another — at the root of stress-induced generalized fear.
Studying the brains of mice in an area known as the dorsal raphe (located in the brainstem), the researchers found that acute stress induced a switch in the chemical signals in the neurons, flipping from excitatory “glutamate” to inhibitory “GABA” neurotransmitters, which led to generalized fear responses.
“Our results provide important insights into the mechanisms involved in fear generalization,” said Spitzer, a member of UC San Diego’s Department of Neurobiology and Kavli Institute for Brain and Mind. “The benefit of understanding these processes at this level of molecular detail — what is going on and where it’s going on — allows an intervention that is specific to the mechanism that drives related disorders.”
Building upon this new finding of a stress-induced switch in neurotransmitters, considered a form of brain plasticity, the researchers then examined the postmortem human brains of individuals who had suffered from PTSD. A similar glutamate-to-GABA neurotransmitter switch was confirmed in their brains as well.
The researchers next found a way to stop the production of generalized fear. Prior to the experience of acute stress, they injected the dorsal raphe of the mice with an adeno-associated virus (AAV) to suppress the gene responsible for synthesis of GABA. This method prevented the mice from acquiring generalized fear.
Further, when mice were treated with the antidepressant fluoxetine (branded as Prozac) immediately after a stressful event, the transmitter switch and subsequent onset of generalized fear were prevented.
Not only did the researchers identify the location of the neurons that switched their transmitter, but they demonstrated the connections of these neurons to the central amygdala and lateral hypothalamus, brain regions that were previously linked to the generation of other fear responses.
“Now that we have a handle on the core of the mechanism by which stress-induced fear happens and the circuitry that implements this fear, interventions can be targeted and specific,” said Spitzer.
An image of the dorsal raphe, an area located in the brainstem, shows serotonergic neurons in green, a virally expressed TdTomato protein in red and colocalized cells in yellow. Spitzer Lab, UC San Diego
The dorsal raphe area of the brain is imaged using confocal microscopy.
The dorsal raphe area of the brain is imaged using confocal microscopy.
CREDIT
Spitzer Lab, UC San Diego
Spitzer Lab, UC San Diego
JOURNAL
Science
METHOD OF RESEARCH
Experimental study
SUBJECT OF RESEARCH
Animals
ARTICLE TITLE
Generalized fear after acute stress is caused by change in neuronal co-transmitter identity
ARTICLE PUBLICATION DATE
15-Mar-2024
Abnormal brain structure identified in children with developmental language problems
WASHINGTON – A rigorous analysis of numerous studies concludes that a part of the brain traditionally associated with movement is abnormal in children with developmental language impairments, according to Georgetown University Medical Center neuroscientists. The discovery has the potential to improve both the diagnosis and treatment of the language difficulties.
The researchers investigated brain abnormalities in developmental language disorder. This condition, which impacts the development of various aspects of language, is about as common as attention-deficit/hyperactivity disorder (ADHD) and dyslexia, and more prevalent than autism. The scientists found that abnormalities occurred specifically in the anterior neostriatum within the basal ganglia, a structure found deep in the brain. They describe their findings in Nature Human Behaviour on March 15.
To better understand why the language impairments occur, the researchers analyzed the results of 22 articles examining brain structures in people with the disorder, and then employed a new computational method to identify common patterns of abnormalities across the studies. They determined that the anterior neostriatum was abnormal in 100% of the studies that examined the structure, with fewer abnormalities in all other parts of the brain.
“We hope that by identifying the neural bases of developmental language difficulties we may help increase awareness of a major, but also rather unrecognized, disorder,” says the study’s lead author Michael T. Ullman, PhD, professor of neuroscience and director of the Brain and Language Laboratory at Georgetown University Medical Center. “We caution, however, that further research is necessary to understand exactly how the anterior neostriatum might lead to the language difficulties.”
Ullman says the findings underscore the potential utility of drugs that are known to improve movement impairments due to basal ganglia dysfunction, such as those that act on dopamine receptors. Interventions that encourage compensation by intact brain structures may also be useful. Additionally, basal ganglia abnormalities could potentially serve as early biomarkers of an increased likelihood of developmental language problems. Such early warning signs could trigger further diagnostic procedures, potentially leading to early therapy.
“Continuing research efforts to further understand the neurobiology of developmental language disorder, especially the role of the basal ganglia, could help the many children who are affected by these problems,” concludes Ullman.
###
In addition to Ullman, other authors at Georgetown include Mariel Pullman, Jarrett Lovelett, Xiong Jiang, and Peter Turkeltaub. Gillian Clark was at Deakin University, Melbourne, Australia. Elizabeth Pierpont is at the University of Minnesota Medical Center, Minneapolis.
This work was supported by NIH grants R01 HD049347 and R21 HD 087088; NSF grants BCS 1439290 and BCS 1940980; and funding from the Mabel H. Flory Trust.
The authors declare no personal financial interests related to the study.
About Georgetown University Medical Center
As a top academic health and science center, Georgetown University Medical Center provides, in a synergistic fashion, excellence in education — training physicians, nurses, health administrators and other health professionals, as well as biomedical scientists — and cutting-edge interdisciplinary research collaboration, enhancing our basic science and translational biomedical research capacity in order to improve human health. Patient care, clinical research and education is conducted with our academic health system partner, MedStar Health. GUMC’s mission is carried out with a strong emphasis on social justice and a dedication to the Catholic, Jesuit principle of cura personalis -- or “care of the whole person.” GUMC comprises the School of Medicine, the School of Nursing, School of Health, Biomedical Graduate Education, and Georgetown Lombardi Comprehensive Cancer Center. Designated by the Carnegie Foundation as a doctoral university with "very high research activity,” Georgetown is home to a Clinical and Translational Science Award from the National Institutes of Health, and a Comprehensive Cancer Center designation from the National Cancer Institute. Connect with GUMC on Facebook (Facebook.com/GUMCUpdate) and on Twitter (@gumedcenter).
JOURNAL
Nature Human Behaviour
METHOD OF RESEARCH
Literature review
SUBJECT OF RESEARCH
People
ARTICLE TITLE
The neuroanatomy of developmental language disorder: a systematic review and meta-analysis
ARTICLE PUBLICATION DATE
15-Mar-2024
“Noisy” roundworm brains give rise to individuality
Scientists demonstrate how individual differences in “whole-brain” activity are generated in roundworms
Joint research led by Yu Toyoshima and Yuichi Iino of the University of Tokyo has demonstrated individual differences in and successfully extracted commonalities from the whole-brain activity of roundworms. The researchers also found that computer simulations based on the whole-brain activity of roundworms more accurately reflect real-brain activity when they include so-called “noise,” or probabilistic elements. The findings were published in the journal PLOS Computational Biology.
The roundworm Caenorhabditis elegans is a favorite among neuroscientists because its 302 neurons are completely mapped. This gives a fantastic opportunity to reveal their neural mechanism at a systems level. Thus far, scientists have been making progress in revealing the different states and patterns of each neuron and the assemblies they form. However, how these states and patterns are generated has been a less explored frontier.
First, the team of scientists measured the neural activity of each cell that makes up a primitive brain in the roundworms' head area. To achieve this, the worms were placed in a microfluidic chip, a tiny device designed for worms to be able to “wiggle” backward and forward while keeping them within the field of view of the objective lens. Then, using a confocal microscope, the scientists filmed how the neurons reacted to changes in salt concentrations.
“Although we were able to extract neural “motifs” common among individuals,” Iino says, “we were surprised to find large individual differences in neural activity. Information from sensory neurons is transmitted to “command” neurons through multiple paths to control behavior. Since the neural circuits of C. elegans are thought to be relatively well conserved among individuals, we had assumed that there would be little variation in these paths among individuals. But remarkably, we found the opposite.”
The data derived from these “films” of roundworm brains were then used to create computer simulations of roundworm brains. However, the first simulations that contained only deterministic elements generated decaying “neural” activity. By adding “noise” to the models, the team achieved an accurate representation of the roundworms’ whole-brain activity. The scientists were not only able to estimate the strength of connectivity between neurons but also demonstrated that “noise” is essential to brain activity. This mathematical model could even potentially be applied to analyze neuronal activity in cases where complete connectome data is not yet available.
With such possibilities, the number of exciting, new questions seems infinite. But choose a scientist must.
“We originally designed this study to investigate the neural mechanisms involved when roundworms are attracted to salt," Iino explains. "However, to measure whole-brain activity, we needed to keep the roundworms in a narrow channel so that they would not move away. We would like to improve the microscope so that we can track freely moving roundworms and analyze whole-brain activity while they are being attracted to salt.”
Whole brain visualization [VIDEO] |
A video taken with a confocal microscope of the whole brain of a roundworm
Neural activity motifs (the common elements of brain activity among individual roundworms) and whole-brain simulation based on whole-brain activity
Neural activity motifs (the common elements of brain activity among individual roundworms) and whole-brain simulation based on whole-brain activity
CREDIT
Toyoshima et al 2024
Toyoshima et al 2024
JOURNAL
PLoS Computational Biology
METHOD OF RESEARCH
Experimental study
SUBJECT OF RESEARCH
Animals
ARTICLE TITLE
Ensemble dynamics and information flow deduction from whole-brain imaging data
ARTICLE PUBLICATION DATE
15-Mar-2024
How the brain translates motivation into goal-oriented behavior, according to new study
: In the mouse brain, two neural pathways were discovered: The first is active during motivation; the second is active only at the termination of motivation. In humans, these pathways could underlie motivational dysfunctions present in various psychiatric
BIRMINGHAM, Ala. – Hunger can drive a motivational state that leads an animal to a successful pursuit of a goal — foraging for and finding food.
In a highly novel study published in Current Biology, researchers at the University of Alabama at Birmingham and the National Institute of Mental Health, or NIMH, describe how two major neuronal subpopulations in a part of the brain’s thalamus called the paraventricular nucleus participate in the dynamic regulation of goal pursuits. This research provides insight into the mechanisms by which the brain tracks motivational states to shape instrumental actions.
For the study, mice first had to be trained in a foraging-like behavior, using a long, hallway-like enclosure that had a trigger zone at one end and a reward zone at the other end, more than 4 feet distant.
Mice learned to wait in a trigger zone for two seconds, until a beep triggered initiation of their foraging-like behavioral task. A mouse could then move forward at its own pace to the reward zone to receive a small gulp of strawberry-flavored Ensure. To terminate the trial, the mice needed to leave the reward zone and return to the trigger area, to wait for another beep. Mice learned quickly and were highly engaged, as shown by completing a large volume of trials during training.
The researchers then used optical photometry and the calcium sensor GCaMP to continuously monitor activity of two major neuronal subpopulations of the paraventricular nucleus, or PVT, during the reward approach from the trigger zone to the reward zone, and during the trial termination from the reward zone back to the trigger zone after a taste of strawberry-flavored food. The experiments involve inserting an optical fiber into the brain just about the PVT to measure calcium release, a signal of neural activity.
The two subpopulations in the paraventricular nucleus are identified by presence or absence of the dopamine D2 receptor, noted as either PVTD2(+) or PVTD2(–), respectively. Dopamine is a neurotransmitter that allows neurons to communicate with each other.
“We discovered that PVTD2(+) and PVTD2(–) neurons encode the execution and termination of goal-oriented actions, respectively,” said Sofia Beas, Ph.D., assistant professor in the UAB Department of Neurobiology and a co-corresponding author of the study. “Furthermore, activity in the PVTD2(+) neuronal population mirrored motivation parameters such as vigor and satiety.”
Specifically, the PVTD2(+) neurons showed increased activity during the reward approach and decreased activity during trial termination. Conversely, PVTD2(–) neurons showed decreased activity during the reward approach and increased activity during trial termination.
“This is novel because people didn’t know there was diversity within the PVT neurons,” Beas said. “Contrary to decades of belief that the PVT is homogeneous, we found that, even though they are the same types of cells (both release the same neurotransmitter, glutamate), PVTD2(+) and PVTD2(–) neurons are doing very different jobs. Additionally, the findings from our study are highly significant as they help interpret contradictory and confusing findings in the literature regarding PVT’s function.”
For a long time, the thalamic areas such as the PVT had been considered just a relay station in the brain. Researchers now realize, Beas says, that the PVT instead processes information, translating hypothalamic-derived needs states into motivational signals via projections of axons — including the PVTD2(+) and PVTD2(–) axons — to the nucleus accumbens, or NAc. The NAc has a critical role in the learning and execution of goal-oriented behaviors. An axon is a long cable-like extension from a neuron cell body that transfers the neuron’s signal to another neuron.
Researchers showed that these changes in neuron activity at the PVT were transmitted to the NAc by measuring neural activity with an optical fiber inserted where the terminals of the PVT axons reach the NAc neurons. The activity dynamics at the PVT-NAc terminals largely mirrored the activity dynamics the researchers saw at the PVT neurons — namely increased neuron activity signal of PVTD2(+) during reward approach and increased neuron activity of PVTD2(–) during trial termination.
“Collectively, our findings strongly suggest that motivation-related features and the encoding of goal-oriented actions of posterior PVTD2(+) and PVTD2(-) neurons are being relayed to the NAc through their respective terminals,” Beas said.
During each mouse recording session, the researchers recorded eight to 10 data samples per second, resulting in a very big dataset. In addition, these types of recordings are subject to many potential confounding variables. As such, the analysis of this data was another novel aspect of this study, through use of a new and robust statistical framework based on Functional Linear Mixed Modeling that both account for the variability of the recordings and can explore the relationships between the changes of photometry signals over time and various co-variates of the reward task, such as how quickly mice performed a trial, or how the hunger levels of the animals can influence the signal.
One example of how researchers correlated motivation with task performance was separating the trial times into “fast” groups, two to three seconds to the reward zone from the trigger zone, and “slow” groups, nine to 11 seconds to the reward zone.
“Our analyses showed that reward approach was associated with higher calcium signal ramps in PVTD2(+) neurons during fast compared to slow trials,” Beas said. “Moreover, we found a correlation between signal and both latency and velocity parameters. Importantly, no changes in posterior PVTD2(+) neuron activity were observed when mice were not engaged in the task, as in the cases where mice were roaming around the enclosure but not actively performing trials. Altogether, our findings suggest that posterior PVTD2(+) neuron activity increases during reward-seeking and is shaped by motivation.”
Deficits in motivation are associated with psychiatric conditions like substance abuse, binge eating and the inability to feel pleasure in depression. A deeper understanding of the neural basis of motivated behavior may reveal specific neuronal pathways involved in motivation and how they interact. This could lead to new therapeutic targets to restore healthy motivational processes in patients.
Co-authors with Beas in the study, “Dissociable encoding of motivated behavior by parallel thalamo-striatal projections,” are Isbah Khan, Claire Gao, Gabriel Loewinger, Emma Macdonald, Alison Bashford, Shakira Rodriguez-Gonzalez, Francisco Pereira and Mario Penzo, NIMH, Bethesda, Maryland. Beas was a post-doctoral fellow at the NIMH before moving to UAB last year.
Support came from National Institutes of Health award K99/R00 MH126429, a NARSAD Young Investigator Award by the Brain and Behavior Research Foundation, and NIMH Intramural Research Program award 1ZIAMH002950.
At UAB, Neurobiology is a department in the Marnix E. Heersink School of Medicine.
JOURNAL
Current Biology
METHOD OF RESEARCH
Experimental study
SUBJECT OF RESEARCH
Animals
ARTICLE TITLE
Dissociable encoding of motivated behavior by parallel thalamo-striatal projections
ARTICLE PUBLICATION DATE
14-Mar-2024
Fatty food before surgery may impair memory in old, young adults
Study in rats also finds omega-3 supplement reduces effects
OHIO STATE UNIVERSITY
COLUMBUS, Ohio – Eating fatty food in the days leading up to surgery may prompt a heightened inflammatory response in the brain that interferes for weeks with memory-related cognitive function in older adults – and, new research in animals suggests, even in young adults.
The study, building upon previous research from the same lab at The Ohio State University, also showed that taking a DHA omega-3 fatty acid supplement for a month before the unhealthy eating and surgical procedure prevented the effects on memory linked to both the high-fat diet and the surgery in aged and young adult rats.
Three days on a high-fat diet alone was detrimental to a specific type of fear-related memory in aged rats for as long as two weeks later – the same type of impairment seen in younger rats that ate fatty food and had a surgical procedure. The team has traced the brain inflammation behind these effects to a protein that activates the immune response.
“These data suggest that these multiple insults have a compounding effect,” said senior author Ruth Barrientos, an investigator in Ohio State’s Institute for Behavioral Medicine Research and associate professor of psychiatry and behavioral health and neuroscience in the College of Medicine.
“We’ve shown that an unhealthy diet, even in the short term, especially when it’s consumed so close to a surgery, which in and of itself will cause an inflammatory response, can have damaging results,” Barrientos said. “The high-fat diet alone might increase inflammation in the brain just a little bit, but then you have surgery that does the same thing, and when put together in a short amount of time you get a synergistic response that can set things in motion toward a longer-term memory issue.”
The study was published recently in the journal Brain, Behavior, and Immunity.
Barrientos’ lab studies how everyday life events might trigger inflammation in the aging brain as the nervous system responds to signals from the immune system reacting to a threat. Decades of research has suggested that with aging comes long-term “priming” of the brain’s inflammatory profile and a loss of brain-cell reserve to bounce back.
Researchers fed young adult and aged rats a diet high in saturated fat for three days before a procedure resembling exploratory abdominal surgery – an event already known to cause about a week of cognitive issues in an older brain. Control rats ate regular food and were anesthetized, but had no surgery. (Barrientos’ lab has determined anesthesia alone does not cause memory problems in rats.)
In this study, as in previous research on aged rats treated with morphine after surgery, the team showed that an immune system receptor called TLR4 was the culprit behind the brain inflammation and related memory problems generated by both surgery and the high-fat diet, said first author Stephanie Muscat, assistant clinical professor of neuroscience at Ohio State.
“Blocking the TLR4 signaling pathway prior to the diet and surgery completely prevented that neuroimmune response and memory impairments, which confirmed this specific mechanism,” Muscat said. “And as we had found before in another model of an unhealthy diet, we showed that DHA supplementation did mitigate those inflammatory effects and prevent memory deficits after surgery.”
There were some surprising memory findings in the new work. Different behavioral tasks are used to test two types of memory: contextual memory based in the hippocampus and cued-fear memory based in the amygdala. In contextual memory tests, rats with normal memory freeze when they re-enter a room in which they had an unpleasant experience. Cued-fear memory is evident when rats freeze in a new environment when they hear a sound connected to that previous bad experience.
For aged rats in this study, as expected, the combination of a high-fat diet and surgery led to problems with both contextual and cued-fear memory that persisted for at least two weeks – a longer-lasting effect than the researchers had seen before.
The high-fat diet alone also impaired the aging rats’ cued-fear memory. And in young adult rats, the combination of the high-fat diet and surgery led to only cued-fear memory deficits, but no problems with memory governed by the hippocampus.
“What this is telling us in aged animals, along with the fact we’re seeing this same impairment in young animals after the high-fat diet and surgery, is that cued-fear memory is uniquely vulnerable to the effects of diet. And we don’t know why,” Barrientos said. “One of the things we’re hoping to understand in the future is the vulnerability of the amygdala to these unhealthy diet challenges.”
With increasing evidence suggesting that fatty and highly processed foods can trigger inflammation-related memory problems in brains of all ages, the consistent findings that DHA – one of two omega-3 fatty acids in fish and other seafood and available in supplement form – has a protective effect are compelling, Barrientos said.
“DHA was really effective at preventing these changes,” she said. “And that’s amazing – it really suggests that this could be a potential pretreatment, especially if people know they’re going to have surgery and their diet is unhealthy.”
This work was supported by grants from the National Institute on Aging and the National Institute of Neurological Disorders and Stroke.
Co-authors included Michael Butler, Menaz Bettes, James DeMarsh, Emmanuel Scaria and Nicholas Deems, all of Ohio State.
#
Contacts:
Ruth Barrientos, ruth.barrientos@osumc.edu
Stephanie Muscat, stephanie.muscat@osumc.edu
Written by Emily Caldwell, Caldwell.151@osu.edu; 614-292-8152
JOURNAL
Brain Behavior and Immunity
METHOD OF RESEARCH
Experimental study
SUBJECT OF RESEARCH
Animals
ARTICLE TITLE
Post-operative cognitive dysfunction is exacerbated by high-fat diet via TLR4 and prevented by dietary DHA supplementation
Genome-wide transcriptome profiling and development of age prediction models in the human brain
“Our approach identified genes that were previously implicated in aging, as well as new ones that may warrant further investigation.”
BUFFALO, NY- March 15, 2024 – A new research paper was published on the cover of Aging (listed by MEDLINE/PubMed as "Aging (Albany NY)" and "Aging-US" by Web of Science) Volume 16, Issue 5, entitled, “Genome-wide transcriptome profiling and development of age prediction models in the human brain.”
Aging-related transcriptome changes in various regions of the healthy human brain have been explored in previous works, however, a study to develop prediction models for age based on the expression levels of specific panels of transcripts is lacking. Moreover, studies that have assessed sexually dimorphic gene activities in the aging brain have reported discrepant results, suggesting that additional studies would be advantageous. The prefrontal cortex (PFC) region was previously shown to have a particularly large number of significant transcriptome alterations during healthy aging in a study that compared different regions in the human brain.
In this new study, researchers Joseph A. Zarrella and Amy Tsurumi from the Harvard T.H. Chan School of Public Health, Massachusetts General Hospital, Harvard Medical School, and Shriner's Hospitals for Children-Boston aimed to profile PFC transcriptome changes during healthy human aging overall and comparing potential differences between female and male samples, as well as developing chronological age prediction models by various methods.
“We harmonized neuropathologically normal PFC transcriptome datasets obtained from the Gene Expression Omnibus (GEO) repository, ranging in age from 21 to 105 years, and found a large number of differentially regulated transcripts in the old and elderly, compared to young samples overall, and compared female and male-specific expression alterations.”
The team assessed the genes that were associated with age by employing ontology, pathway, and network analyses. Furthermore, they applied various established (least absolute shrinkage and selection operator (Lasso) and Elastic Net (EN)) and recent (eXtreme Gradient Boosting (XGBoost) and Light Gradient Boosting Machine (LightGBM)) machine learning algorithms to develop accurate prediction models for chronological age and validated them. Studies to further validate these models in other large populations and molecular studies to elucidate the potential mechanisms by which the transcripts identified may be related to aging phenotypes would be advantageous.
“Our results support the notions that specific gene expression changes in the PFC are highly correlated with age, that some transcripts show female and male-specific differences, and that machine learning algorithms are useful tools for developing prediction models for age based on transcriptome information.”
Read the full study: DOI: https://doi.org/10.18632/aging.205609
Corresponding Author: Amy Tsurumi - atsurumi@mgh.harvard.edu
Keywords: aging machine learning prediction model biomarker transcriptome
Click here to sign up for free Altmetric alerts about this article.
About Aging:
Aging publishes research papers in all fields of aging research including but not limited, aging from yeast to mammals, cellular senescence, age-related diseases such as cancer and Alzheimer’s diseases and their prevention and treatment, anti-aging strategies and drug development and especially the role of signal transduction pathways such as mTOR in aging and potential approaches to modulate these signaling pathways to extend lifespan. The journal aims to promote treatment of age-related diseases by slowing down aging, validation of anti-aging drugs by treating age-related diseases, prevention of cancer by inhibiting aging. Cancer and COVID-19 are age-related diseases.
Aging is indexed by PubMed/Medline (abbreviated as “Aging (Albany NY)”), PubMed Central, Web of Science: Science Citation Index Expanded (abbreviated as “Aging‐US” and listed in the Cell Biology and Geriatrics & Gerontology categories), Scopus (abbreviated as “Aging” and listed in the Cell Biology and Aging categories), Biological Abstracts, BIOSIS Previews, EMBASE, META (Chan Zuckerberg Initiative) (2018-2022), and Dimensions (Digital Science).
Please visit our website at www.Aging-US.com and connect with us:
- X, formerly Twitter
- YouTube
- Spotify, and available wherever you listen to podcasts
Click here to subscribe to Aging publication updates.
For media inquiries, please contact media@impactjournals.com.
Aging (Aging-US) Journal Office
6666 E. Quaker Str., Suite 1B
Orchard Park, NY 14127
Phone: 1-800-922-0957, option 1
###
JOURNAL
Aging-US
METHOD OF RESEARCH
Data/statistical analysis
SUBJECT OF RESEARCH
People
ARTICLE TITLE
Genome-wide transcriptome profiling and development of age prediction models in the human brain
No comments:
Post a Comment