Researchers see structural changes in genetic material that allow memories to strengthen when remembered.
Category: neuroscience – Page 735
Chiaradia and Lancaster review applications and limitations of brain organoids, placing them in context with other technologies and describing how these methods are heavily informed by in vivo development.
“It was a jaw-dropping moment, for us and for every scientist we told about this so far.”
But what if there’s more to the story? What if the electromagnetic fields generated by, but which are not identical to, the neuroanatomy of the brain, are in fact the primary seat of consciousness? The brain’s fields are generated by various physiological processes in the brain, but primarily by trans-membrane currents moving through neurons. These fields are always oscillating and they come in various speeds, clustered around certain bands, from delta on the lower end at 1–2.5 cycles (oscillations) per second (Hertz) up to gamma at 40–120 cycles per second.
Some neuroscientists have long considered the brain’s oscillating electromagnetic fields to be interesting but merely “epiphenomenal” features of the brain—like a train whistle on a steam-powered locomotive. Electromagnetic fields may just be noise that doesn’t affect the workings of the brain. Koch still seems to lean this way.
A closer look at Stentrode, the Brain Computer Interface that interacts with the brain via blood vessels. Recent paper demonstrating it working in 2 ALS patients.
Han from WrySci HX goes through the very interesting brain computer interface called Stentrode that can let you tweet with your mind. As a BCI, it’s a rival to Neuralink, Kernal, and Openwater. Find out about its background, how it works, why it’s the most unique BCI, and some results from its clinical trials. More below ↓↓↓
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Summary: Study reveals how gene control mechanisms determine the identity of neurons in the embryonic brainstem. A failure in differentiation in developing brainstem neurons can lead to behavioral abnormalities, including ADHD.
Source: University of Helsinki
A recent study at the University of Helsinki reveals how gene control mechanisms define the identity of developing neurons in the brainstem. The researchers also showed that a failure in differentiation of the brainstem neurons leads to behavioural abnormalities, including hyperactivity and attention deficit.
Virgin Hyperloop, the transportation company owned by business magnate Richard Branson, has ambitious plans to build a vacuum tube transportation system that travels over 600 miles per hour.
But before it does so, the company has made the reasonable decision to figure out what traveling that quickly might to do the brain. To wit, scientists at West Virginia’s Rockefeller Neurosciences Institute (RNI) will find out what to expect when launching passengers at 78 percent the speed of sound.
Hold on to your brains!
Many of the fundamental principles in biology and essentially all pathways regulating development were identified in so-called genetics screens. Originally pioneered in the fruit fly Drosophila and the nematode C. elegans, genetic screens involve inactivation of many genes one by one. By analyzing the consequences of gene loss, scientists can draw conclusions about its function. This way, for example, all genes required for formation of a brain can be identified.
Genetic screens can routinely be carried out in flies and worms. In humans, a wealth of knowledge exists about genetic disorders and the consequences of disease-relevant mutations, but their systematic analysis was impossible. Now, the Knoblich lab at IMBA has developed a groundbreaking technique allowing hundreds of genes to be analyzed in parallel in human tissue. They named the new technology CRISPR-LICHT and published their findings in the journal Science.
By using cerebral organoids, a 3D cell culture model for the human brain developed in Jürgen Knoblich’s group at IMBA, hundreds of mutations can now be analyzed for their role in the human brain using CRISPR-LICHT.
Article. I guess having implants directly on the brain isn’t the only way to have a brain to machine interface. The scientists involved in the study found an alternative by picking up signals through the blood vessels.
It’s not as information packed as a direct brain connection, but it’s not as invasive.
I think it would be a good alternative or even complementary to direct brain implants. Interesting. 😃
Electrodes threaded through the blood vessels that feed the brain let people control gadgets with their minds.
While our circadian body clock dictates our preferred rhythm of sleep or wakefulness, a relatively new concept—the epigenetic clock—could inform us about how swiftly we age, and how prone we are to diseases of old age.
People age at different rates, with some individuals developing both characteristics and diseases related to aging earlier in life than others. Understanding more about this so-called ‘biological age’ could help us learn more about how we can prevent diseases associated with age, such as dementia. Epigenetic markers control the extent to which genes are switched on and off across the different cell-types and tissues that make up a human body. Unlike our genetic code, these epigenetic marks change over time, and these changes can be used to accurately predict biological age from a DNA sample.
Now, scientists at the University of Exeter have developed a new epigenetic clock specifically for the human brain. As a result of using human brain tissue samples, the new clock is far more accurate than previous versions, that were based on blood samples or other tissues. The researchers hope that their new clock, published in Brain and funded by Alzheimer’s Society, will provide insight into how accelerated aging in the brain might be associated with brain diseases such as Alzheimer’s disease and other forms of dementia.
The coronavirus disease 2019 (COVID-19) pandemic does not affect everyone equally. While anyone can contract COVID-19, accumulating data suggest that older people or those with pre-existing comorbidities are far more likely to have severe complications or die from the disease. While researchers scramble to unravel the mechanisms of action underlying the disease’s wide-ranging effects, news that the disease hits older people hardest has been received without demur: it is widely accepted that to be old is to be fragile. Indeed, even in so-called normal times, everyone expects more things break as people age: bones, hearts, brains. In the context of the pandemic, being old is seen as just one more comorbidity.
It should not be.
We accept growing old and losing our vitality as an inevitability of life. To do so is to overlook the fact that ageing is, fundamentally, a plastic trait—influenced both by our genetic predispositions and many (controllable) environmental factors. Anecdotally we know this to be true: for some, being in their eighties means being confined to a wheelchair whereas for others, like Eileen Noble, who at 84 years old was the oldest runner in 2019’s London Marathon, it decidedly does not. The burgeoning field of biogerontology is now beginning to amass data in support of such observations. Single genetic mutations in evolutionarily conserved pathways across model organisms—ranging from fruit flies to mice—increase lifespan by up to 80%. Crucially, not only do these animals live longer, they also have a longer youthspan—the proportion of their lives in which they retain the trappings of youth such as peak mobility, immunity, and stress resilience.