For several years, Jimo Borjigin, a professor of neurology at the University of Michigan, had been troubled by the question of what happens to us when we die.
New research into the dying brain suggests the line between life and death may be less distinct than previously thought by Alex Blasdel.
Electroconvulsive therapy is more effective than ketamine at treating severe depression, according to a new meta-analysis.
Professor Jürgen Götz and Dr Pranesh Padmanabhan from the Queensland Brain Institute comment on the successful human trial by the WVU Rockefeller Neuroscience Institute which found a five-fold reduction of amyloid-β in Alzheimer’s patients.
The latest trial results underscore the safety of using…
Continue reading “The potential of ultrasound and antibodies for Alzheimer’s disease therapy” »
😗😁😘 year 2023.
The world’s first supercomputer capable of simulating networks at the scale of the human brain has been announced by researchers at the International Centre for Neuromorphic Systems (ICNS) at Western Sydney University.
DeepSouth uses a neuromorphic system which mimics biological processes, using hardware to efficiently emulate large networks of spiking neurons at 228 trillion synaptic operations per second — rivalling the estimated rate of operations in the human brain.
Mental health chatbots can help treat symptoms of depression, according to findings from an NTU research team. These apps can interact with people to show empathy and encouragement, to improve moods. CNA spoke to Dr Laura Martinengo, Research Fellow at Lee Kong Chian School of Medicine at NTU.
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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.
