Gene therapies are opening up possibilities that were once reserved for science fiction.
At Harvard University, Professor of Genetics David Sinclair says he believes it’s possible to unlock the fountain of youth, and gene therapy is the key.
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Summary: The genetics of neurocognitive skills were associated with higher tolerance of risk, delayed fertility, less healthy-risk behavior, and a greater willingness to forgo immediate gratification.
Source: Columbia University.
Noncognitive skills and cognitive abilities are both important contributors to educational attainment — the number of years of formal schooling that a person completes — and lead to success across the life course, according to a new study from an international team led by researchers at Columbia University Mailman School of Public Health, the University of Texas at Austin, and Vrije Universiteit Amsterdam.
Octopus and squid make strange evolutionary shortcuts in adaptation. Evolution is an intricate process of change.
According to Science Alert, species of squid and octopus may yet have some surprises in store for us. “In a surprising twist, scientists discovered that octopuses, along with some squid and cuttlefish species, routinely edit their RNA (ribonucleic acid) sequences to adapt to their environment,” the article said.
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The extent to which nonhuman primate vocalizations are amenable to modification through experience is relevant for understanding the substrate from which human speech evolved. We examined the vocal behaviour of Guinea baboons, Papio papio, ranging in the Niokolo Koba National Park in Senegal. Guinea baboons live in a multi-level society, with units nested within parties nested within gangs. We investigated whether the acoustic structure of grunts of 27 male baboons of two gangs varied with party/gang membership and genetic relatedness. Males in this species are philopatric, resulting in increased male relatedness within gangs and parties. Grunts of males that were members of the same social levels were more similar than those of males in different social levels (N = 351 dyads for comparison within and between gangs, and N = 169 dyads within and between parties), but the effect sizes were small. Yet, acoustic similarity did not correlate with genetic relatedness, suggesting that higher amounts of social interactions rather than genetic relatedness promote the observed vocal convergence. We consider this convergence a result of sensory–motor integration and suggest this to be an implicit form of vocal learning shared with humans, in contrast to the goal-directed and intentional explicit form of vocal learning unique to human speech acquisition.
One of the key preconditions for the development of speech is the ability to adjust vocal output in response to auditory input. Humans are exceptionally proficient at vocal learning. Although effortless speech learning is confined to the early years [1], humans still possess the ability to imitate sounds voluntarily and acquire further languages throughout their lives. Numerous comparative studies have aimed at elucidating the evolutionary origins of vocal learning within the primate lineage, to uncover the extent to which nonhuman primates reveal evidence for vocal plasticity, and whether such plasticity may be conceived as a pre-adaptation for the evolution of speech [2, 3].
Despite considerable research effort, it appears that the ability to learn sounds from auditory experience in most nonhuman primate species is limited. Unlike humans or some songbird species, nonhuman primates are not obligatory vocal learners that require species-specific auditory input to develop their normal vocal repertoires [4, 5]. Early attempts to train a young chimpanzee to produce speech sounds yielded disappointing results and prompted most of the ‘ape language’ projects to turn to another modality, using either symbol systems or sign languages [6]. Studies of the neural basis of vocal production in different monkey species found that the animals lack the neural connections necessary for the volitional control over the fine structure of vocalizations, although they exert greater control over the usage of calls (reviewed in [2]).
Biotin is also known as vitamin H, named for the German words “Haar” and “Haut,” which mean hair and skin. This was due to the fact that even slight deficiencies cause hair thinning, skin rash or brittle fingernails. New research, just published in PNAS, now shows that some forms of severe neurodegeneration, like the frontotemporal dementia seen in Alzheimer’s and Parkinson’s, can directly result from lack of sufficient biotin.
The authors discovered this by looking at fruit flies with dementia. Now, before anyone chuckles, fruit flies actually make a nice model of Alzheimer’s or other diseases when they are given the right genes. Human versions of defective MAPT (tau) genes cause these flies to develop tauopathies that resemble those that occur in our own brains. To delve deeper into the neurotoxicity of tau, they looked at over 7000 fly genes in a forward genetic screen before zeroing in on one significantly modified toxicity of the tauR406W mutant. This gene, Btnd, encodes the biotinidase enzyme that extracts biotin from food sources or recycles it from used enzymes.
At the more advanced end of things, genetic modifications and advanced medical procedures might be available in the future that can restore muscle tissue, bone density, and organ health. If such treatments are available down the road, periodic visits to the doctor could allow Loonies to live happy and healthy lives in lower gravity.
In so many ways, a permanent human presence on the Moon could open the door to the entire Solar System. With the ability to refuel and resupply missions from a lunar site, space agencies could shave billions off the cost of deep-space missions. It would also facilitate missions to Mars, Venus, the Asteroid Belt, and beyond.
Cellular senescence, a state of permanent growth arrest, has emerged as a hallmark and fundamental driver of organismal aging. It is regulated by both genetic and epigenetic factors. Despite a few previously reported aging-associated genes, the identity and roles of additional genes involved in the regulation of human cellular aging remain to be elucidated. Yet, there is a lack of systematic investigation on the intervention of these genes to treat aging and aging-related diseases.
How many aging-promoting genes are there in the human genome? What are the molecular mechanisms by which these genes regulate aging? Can gene therapy alleviate individual aging? Recently, researchers from the Chinese Academy of Sciences have shed new light on the regulation of aging.
Recently, researchers from the Institute of Zoology of the Chinese Academy of Sciences (CAS), Peking University, and Beijing Institute of Genomics of CAS have collaborated to identify new human senescence-promoting genes by using a genome-wide CRISPR/Cas9 screening system and provide a new therapeutic approach for treating aging and aging-related pathologies.
Gene-editing method shows promise for premature aging syndrome.
Scientists have fixed a genetic mutation in mice with progeria, a rapid aging disease. The treatment could one day be used in humans who would otherwise die in childhood.
Approximately 1 in 4 million children are diagnosed with progeria within the first two years of birth, and virtually all of these children develop health issues in childhood and adolescence that are normally associated with old age – including cardiovascular disease (heart attacks and strokes), hair loss, skeletal problems, subcutaneous fat loss and hardened skin.
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One mouse is hunched over, graying, and barely moves at 7 months old. Others, at 11 months, have sleek black coats and run around. The videos and other results from a new study have inspired hope for treating children born with progeria, a rare, fatal, genetic disease that causes symptoms much like early aging. In mice with a progeria-causing mutation, a cousin of the celebrated genome editor known as CRISPR corrected the DNA mistake, preventing the heart damage typical of the disease, a research team reports today in. Treated mice lived about 500 days, more than twice as long as untreated animals.
“The outcome is incredible,” says gene-therapy researcher Guangping Gao of the University of Massachusetts, who was not involved with the study.
