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Linking environmental influences, genetic research to address concerns of genetic determinism of human behavior

It has long been known that there is a complex interplay between genetic factors and environmental influences in shaping behavior. Recently it has been found that genes governing behavior in the brain operate within flexible and contextually responsive regulatory networks. However, conventional genome-wide association studies (GWAS) often overlook this complexity, particularly in humans where controlling environmental variables poses challenges.

In a new perspective article published on February 27 in the open-access journal PLOS Biology by researchers from the University of Illinois Urbana-Champaign and Rutgers University, U.S., the importance of integrating environmental effects into genetic research is underscored. The authors discuss how failure to do so can perpetuate deterministic thinking in genetics, as historically observed in the justification of eugenics movements and, more recently, in cases of racially motivated violence.

The authors propose expanding GWAS by incorporating environmental data, as demonstrated in studies on aggression in , in order to get a broader understanding of the intricate nature of gene-environment interactions. Additionally, they advocate for better integration of insights from animal studies into human research. Animal experiments reveal how both genotype and environment shape brain gene regulatory networks and subsequent behavior, and these findings could better inform similar experiments with people.

The 10 Stages of Artificial Intelligence

This definitely is a Lifeboat post embodying what Lifeboat is about, and it’s only about AI. They did a really good job explaining the 10 stages.


This video explores the 10 stages of AI, including God-Like AI. Watch this next video about the Technological Singularity: • Technological Singularity: 15 Ways It…
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How neurotransmitter receptors transport calcium, a process linked with origins of neurological disease

A new study from a team of McGill University and Vanderbilt University researchers is shedding light on our understanding of the molecular origins of some forms of autism and intellectual disability.

For the first time, researchers were able to successfully capture atomic resolution images of the fast-moving ionotropic glutamate receptor (iGluR) as it transports calcium. iGluRs and their ability to transport calcium are vitally important for many brain functions such as vision or other information coming from sensory organs. Calcium also brings about changes in the signaling capacity of iGluRs and nerve connections, which are key cellular events that lead to our ability to learn new skills and form memories.

IGluRs are also key players in and their dysfunction through has been shown to give rise to some forms of autism and intellectual disability. However, basic questions about how iGluRs trigger biochemical changes in the brain’s physiology by transporting calcium have remained poorly understood.

Ancient retroviruses played a key role in the evolution of vertebrate brains, suggest researchers

Researchers report in the journal Cell that ancient viruses may be to thank for myelin—and, by extension, our large, complex brains.

The team found that a retrovirus-derived genetic element or “retrotransposon” is essential for myelin production in mammals, amphibians, and fish. The , which they dubbed “RetroMyelin,” is likely a result of ancient viral infection, and comparisons of RetroMyelin in mammals, amphibians, and fish suggest that retroviral infection and genome-invasion events occurred separately in each of these groups.

“Retroviruses were required for vertebrate evolution to take off,” says senior author and neuroscientist Robin Franklin of Altos Labs-Cambridge Institute of Science. “If we didn’t have retroviruses sticking their sequences into the vertebrate genome, then myelination wouldn’t have happened, and without myelination, the whole diversity of vertebrates as we know it would never have happened.”

Risk Factors for Young-Onset Dementia

Investigators identified 15 factors that affect risk for young-onset dementia.


Limited data are available on risk factors for young-onset dementia. In this study, researchers assessed 39 potential risk factors for young-onset dementia from data in the UK Biobank. Participants 65 years of age or older without a dementia diagnosis were included in the analysis. Potential risk factors were grouped into sociodemographic factors, genetic factors, lifestyle factors, environmental factors, blood marker factors, cardiometabolic factors, psychiatric factors, and other risk factors.

Among 359,052 participants, the mean age at baseline was 55 years and 55% were women. There were 485 incident all-cause young-onset dementia cases after a mean follow-up of 8 years. Incident young-onset dementia increased with age and was more common in men. Fewer years of formal education, lower socioeconomic status, the presence of two apolipoprotein E ℇ4 alleles, no alcohol use, alcohol use disorder, social isolation, vitamin D deficiency (1 mg/dL), lower handgrip strength, hearing impairment, orthostatic hypotension, stroke, diabetes, heart disease, and depression were associated with higher risk for young-onset dementia in fully adjusted models. Men with diabetes were more likely to have young-onset dementia than men without diabetes, and women with high C-reactive protein were more likely to have young-onset dementia than women with low C-reactive protein levels.

The Last Piece of Our Genome: Sequencing the Y Chromosome

Groundbreaking research led by a global group of over 100 researchers will enable a more in-depth exploration of human genetic variation as fully sequencing the Y chromosome, a feat that has challenged scientists for years, has been accomplished for the first time. In this interview, we speak to Dylan Taylor about this impactful research and how it may shape our understanding of human genetics.

Please could you introduce yourself and your current research activities?

I am Dylan Taylor, a Ph.D. candidate and NIH F31 fellow in the Department of Biology at Johns Hopkins University. My work with the T2T consortium focuses on exploring how a complete reference genome can improve our ability to study human genetic variation and how it impacts human traits and health.

Healthy eating and activity reverse aging marker in kids with obesity, Stanford Medicine-led study finds

A genetic marker linked to premature aging was reversed in children with obesity during a six-month diet and exercise program, according to a recent study led by the Stanford School of Medicine.

Children’s telomeres — protective molecular “caps” on the chromosomes — were longer during the weight management program, then were shorter again in the year after the program ended, the study found. The research was published last month in Pediatric Obesity.

Like the solid segment at the end of a shoelace, telomeres protect the ends of chromosomes from fraying. In all people, telomeres gradually shorten with aging. Various conditions, including obesity, cause premature shortening of the telomeres.

Genetic variants, neurocognitive outcomes, and functional neuroimaging in survivors of childhood acute lymphoblastic leukemia

A study involving long-term acute lymphoblastic leukemia (ALL) survivors found certain genetic variants related to the folate pathway, glucocorticoid regulation, and other factors were associated with impaired attention, motor skills, memory, and more. Read the article here:


Genetic predispositions may modulate risk for developing neurocognitive late effects in childhood acute lymphoblastic leukemia (ALL) survivors.

Methods.

Long-term ALL survivors (n = 212; mean = 14.3 [SD = 4.77] years; 49% female) treated with chemotherapy completed neurocognitive testing and task-based functional neuroimaging. Based on previous work from our team, genetic variants related to the folate pathway, glucocorticoid regulation, drug metabolism, oxidative stress, and attention were included as predictors of neurocognitive performance, using multivariable models adjusted for age, race, and sex. Subsequent analyses evaluated the impact of these variants on task-based functional neuroimaging. Statistical tests were 2-sided.

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