Closed-loop electrical stimulation of the internal capsule of participants undergoing intracranial epilepsy monitoring improved the participants’ performance on a cognitive conflict task, and performance could be decoded from electrode activity.
Two progressively degenerative diseases, amyotrophic lateral sclerosis (ALS, commonly known as Lou Gehrig’s disease) and frontotemporal dementia (FTD, recently in the news with the diagnoses of actor Bruce Willis and talk show host Wendy Williams), are linked by more than the fact that they both damage nerve cells critical to normal functioning—the former affecting nerves in the brain and spinal cord leading to loss of movement, the latter eroding the brain regions controlling personality, behavior and language.
Research studies have repeatedly shown that in patients with ALS or FTD, the function of TAR DNA-binding protein 43, more commonly called TDP-43, becomes corrupted. When this happens, pieces of the genetic material called ribonucleic acid (RNA) can no longer be properly spliced together to form the coded instructions needed to direct the manufacture of other proteins required for healthy nerve growth and function.
The RNA strands become riddled with erroneous code sequences called “cryptic exons” that instead affect proteins believed to be associated with increased risk for ALS and FTD development.
When a long-term memory forms, some brain cells experience a rush of electrical activity so strong that it snaps their DNA. Then, an inflammatory response kicks in, repairing this damage and helping to cement the memory, a study in mice shows. The findings, published on 27 March in Nature1, are “extremely exciting”, says Li-Huei Tsai, a neurobiologist at the Massachusetts Institute of Technology in Cambridge who was not involved in the work. They contribute to the picture that forming memories is a “risky business”, she says. Normally, breaks in both strands of the double helix DNA molecule are associated with diseases including cancer. But in this case, the DNA damage-and-repair cycle offers one explanation for how memories might form and last.
It also suggests a tantalizing possibility: this cycle might be faulty in people with neurodegenerative diseases such as Alzheimer’s, causing a build-up of errors in a neuron’s DNA, says study co-author Jelena Radulovic, a neuroscientist at the Albert Einstein College of Medicine in New York City.
Alzheimer’s is the most common form of dementia, affecting an estimated 6.7 million people in the US. Researchers seeking an effective treatment for the affliction have, over the last 30 years, focused their efforts on a protein known as amyloid beta (A-beta), which form clumps in the brain.
These clumps of A-beta proteins attack nerve cells, resulting initially in short-term memory impairment and later in the loss of judgment, language and thought processes.
Other researchers have previously developed an antibody which can identify and attach itself to A-beta proteins and delay the progression of Alzheimer’s in patients with early-to-mild cognitive impairment by up to 36%.
The survival of neurons, unlike most other cells in the body, depends largely on the energy provided by mitochondria, intracellular organelles that contain their DNA to function properly.
Transcranial magnetic stimulation (TMS) appears to relieve depression by correcting brain signals that are traveling the wrong direction.
New research suggests that there is no ‘typical’ form of Alzheimer’s disease, as the condition can manifest in at least four different ways.
Very interesting article.
Now a physicist working at the University of Portsmouth in the UK has published research in the AIP Advances journal that he says provides support to the strange theory.
“I don’t want to paraphrase Morpheus from The Matrix but he said ‘what is real?’” the Associate Professor of Physics, Dr Melvin Vopson, said.
Continue reading “Physicist says his study supports computer simulation theory” »
When a positive voltage was applied to the chip, the ions flowed to the pore, where their pressure created a blister between the chip’s surface and the graphite layer. When the blister forced the graphite upward, the device became more conductive, switching its memory state to “on.” Since the graphite stayed lifted even without a current, the chip essentially remembered this state, A negative voltage could pull the chip’s layers back together, resetting the device to its “off” state.
The scientists were able to connect two of these chips to form a logic gate —a circuit that can implement logical operations such as AND, OR, and NOT. They note they can build any other classical logic gate commonly employed in digital computing using their logic gate. This is the first time multiple fluidic memristors have been connected to form a circuit.
Previously, scientists developed fluidic memristors based on tiny syringes or microscopic slits. However, these earlier devices were too bulky and complex to scale up to larger systems. In contrast, the new microchips are compact and scalable, Emmerich says.
