?kh=-1&uddg= If you are looking forward to your first stiff drink after a dry January, be warned: it may feel bittersweet. You may feel you deserve an alcoholic beverage after toughing it out all month – but have you forgotten what it feels like to wake up haunted by worries about what you said or did the night before? These post-drinking feelings of guilt and stress have come to be known colloquially as “hangxiety”. But what causes them? David Nutt, professor of neuropsychopharmacology at Imperial College, London, is the scientist who was fired in 2009 as the government’s chief drug adviser for saying alcohol is more dangerous than ecstasy and LSD. Alcohol, he says, targets the Gaba (gamma-aminobutyric acid) receptor, which sends chemical messages through the brain and central nervous system to inhibit the activity of nerve cells. The first two drinks lull you into a blissful Gaba-induced state of chill. The body registers this new imbalance in brain chemicals and attempts to put things right.
Novel discovery offers hope for treatment of Alzheimer's and other neurological diseases August 10, 2018 There is new hope for the treatment of Alzheimer's and other neurological diseases following a ground-breaking discovery made by an Australian-Chinese research collaboration. Researchers from the University of South Australia and the Third Military Medical University in China have discovered a signal pathway within cells, and also invented a potential drug that could stop degeneration and actually improve learning and memory in affected patients. UniSA's Professor Xin-Fu Zhou and colleagues have been investigating tauopathies – which refers to a class of diseases caused by misfolding of the tau protein inside nerve cells that results in cell damage and eventually cell death. These diseases include Alzheimer's, Parkinson's and Motor Neuron Disease, all of which presently have no cure. "Right now there is no treatment available at all," Prof Zhou says.
Bizarre Discovery Shows Your Bones Could Be Triggering The 'Fight-or-Flight' Response When faced with a threat, hormones flood our bodies in preparation either for battle or a quick escape - what's commonly known as the 'fight-or-flight' response. For decades, we've generally thought this response was driven by hormones such as adrenaline. But it now seems that one of the most important of these messengers could come from a rather unexpected place – our skeleton. We usually think of chemicals like cortisol and adrenaline as the things that get the heart racing and muscles pumping. But the real star player could actually be osteocalcin, a calcium-binding protein produced by our bones. As a response to acute stress, steroids of the glucocorticoid variety are released by the body's endocrine system, where they manage the production of a cascade of other 'get ready to rumble' chemicals throughout various tissues. Researchers from the US, the UK, and India argue there's one tiny problem with this explanation of the fight-or-flight reaction.
What Happens When You Spend a Year Using Science to Improve Your Brain - The Verge - Pocket Illustration James Bareham / The Verge Here are two things that are both true. Neuroplasticity is real — that is, the brain really can change and learn and improve based on experience. And there’s little evidence that brain-training games are any better than placebo. “So,” wondered science journalist Caroline Williams, “if brain training isn’t the way to apply it, what should we be doing?” The Verge spoke to Williams about her expectations, more successful (and failed) experiments, and how to avoid the hype. Photo: Ann Ayerst What was your approach going into these experiments? I went with an open mind. One of the poster children for neuroplasticity are the London taxi drivers, and studies show that as taxi drivers learn to navigate the streets and memorize the routes, the hippocampus — the part of the brain that does spatial navigation — gets larger. Of the three brain areas that are activated when you make sense of place, two of them were normal and one just didn’t respond at all.
New leads on treating dementia and Alzheimer's A new study by scientists in Australia and the US provides an explanation for why clinical trials of drugs targeting proteins in the brain that were thought to cause dementia and Alzheimer's have failed. The study has opened the way for potential new treatments with existing drugs. Published online in the journal Human Molecular Genetics, the researchers assembled evidence from a wide range of human studies and animal models of dementia-related diseases to show that inflammation is a major cause, not just a consequence. They show that many genes linked with dementia regulate our susceptibility and response to inflammatory damage. "For decades, scientists have thought that dementia and Alzheimer's Disease are caused by protein aggregates forming in the brain. Inflammation has long been known to increase as dementia-related diseases progress, but only now is it identified as the cause. The new work turns previous thinking around. He likens the brain inflammation to a virus infection.
Cause of antibiotic resistance identified Scientists have confirmed for the first time that bacteria can change form to avoid being detected by antibiotics in the human body. Studying samples from elderly patients with recurring urinary tract infections, the Newcastle University team used state-of-the art techniques to identify that a bacteria can lose its cell wall—the common target of many groups of antibiotics. The research by the Errington lab which turns on its head current thinking about the bacteria's ability to survive without a cell wall, known as "L-form switching", is published today in Nature Communications. The World Health Organisation has identified antibiotic resistance as one of the biggest threats to global health, food security, and development today. Lead author, Dr. "In this form the body can't easily recognise the bacteria so doesn't attack them—and neither do antibiotics." L-form—flimsy but survives In this L-form the bacteria are flimsy and weaker but some survive, hiding inside the body. Dr. Diagnosis
The Empty Brain - aeon - Pocket No matter how hard they try, brain scientists and cognitive psychologists will never find a copy of Beethoven’s 5th Symphony in the brain – or copies of words, pictures, grammatical rules or any other kinds of environmental stimuli. The human brain isn’t really empty, of course. But it does not contain most of the things people think it does – not even simple things such as ‘memories’. Our shoddy thinking about the brain has deep historical roots, but the invention of computers in the 1940s got us especially confused. To see how vacuous this idea is, consider the brains of babies. A healthy newborn is also equipped with more than a dozen reflexes – ready-made reactions to certain stimuli that are important for its survival. Senses, reflexes and learning mechanisms – this is what we start with, and it is quite a lot, when you think about it. We don’t store words or the rules that tell us how to manipulate them. Humans, on the other hand, do not – never did, never will.
Is ‘friendly fire’ in the brain provoking Alzheimer’s disease? Neuroscientist Michael Heneka knows that radical ideas require convincing data. In 2010, very few colleagues shared his belief that the brain’s immune system has a crucial role in dementia. So in May of that year, when a batch of new results provided the strongest evidence he had yet seen for his theory, he wanted to be excited, but instead felt nervous. He and his team had eliminated a key inflammation gene from a strain of mouse that usually develops symptoms of Alzheimer’s disease. Even he was surprised how well the mice fared; he had expected that removal of the gene, known as Nlpr3, would protect their brains a little, but not that it would come close to preventing dementia symptoms. He reanalysed the results again and again. Over the next couple of years, he confirmed that nothing had gone wrong with the experiments. But there are roadblocks ahead. Clogged and swollen In 2013, microglia began to loom large in Alzheimer’s disease research. Neuroscientists started to pay attention.