Lifeboat Foundation

AI is spreading beyond the tech giants into all aspects of life and work. One of its most impactful roles will be to help nuclear medicine save the lives of many thousands of cancer patients.

A recent study has suggested that transcriptomes may be the best method for classifying different types of brain disease.

Brains are like puzzles, requiring many nested and co-dependent pieces to function well. The brain is divided into areas, each containing many millions of neurons connected across thousands of synapses. These synapses, which enable communication between neurons, depend on even smaller structures: message-sending boutons (swollen bulbs at the branch-like tips of neurons), message-receiving dendrites (complementary branch-like structures for receiving bouton messages), and power-generating mitochondria. To create a cohesive brain, all these pieces must be accounted for.

However, in the aging brain, these pieces can get lost or altered, and no longer fit in the greater brain puzzle. A research team has now published a study in Frontiers in Aging Neuroscience on this topic.

“Fifty percent of people experience loss of working memory with old age, meaning their ability to hold and manipulate information in the short-term decreases,” says co-first author Courtney Glavis-Bloom, a senior staff scientist in Salk Institute Professor John Reynolds’s lab. “We set out to understand why some individuals maintain healthy working memory as they age, while others do not. In the process, we discovered a novel mechanism for the synaptic basis of cognitive impairment.”

Functional movement/conversion disorder (FMD), part of the spectrum of Functional Neurological Disorder (FND), is a neuropsychiatric condition marked by a range of neurological symptoms, including tremors, muscular spasms and cognitive difficulties. Despite being the second-most common cause of referrals to neurology outpatient clinics after headache, scientists have struggled to pin down the disorder’s root cause. Female sex and a history of childhood trauma are factors associated with higher risk of developing FMD, but it’s been unclear why.

A new study from investigators of the Brigham and Women’s Hospital, in collaboration with researchers at the National Institute of Neurological Disorders and Stroke, demonstrated that FMD is characterized by epigenetic changes, and that women and childhood abuse survivors with FMD have different epigenetic profiles linked to this condition. Their study, which examined the genomes of over 100 individuals and was recently published in Progress in Neuro-Psychopharmacology and Biological Psychiatry, is the first to demonstrate the occurrence of epigenetic changes in FMD.

“This study finally takes FMD out of a cloud of confusion and provides a neuroscientifically grounded explanation for why childhood trauma and female sex are associated with this disorder,” said lead author Primavera A. Spagnolo, MD, Ph.D., scientific director of the Mary Horrigan Connors Center for Women’s Health and Gender Biology and assistant professor of psychiatry at HMS.

In a large study led by the MHH neurology department, researchers investigated the cognition of patients with the rare disease NMOSD. It was found that about 20 percent of those affected have limited cognitive abilities.

People with the rare neuromyelitis optica spectrum disease (NMOSD) have severe physical and psychological impairments. But do they also suffer from limitations in their cognitive abilities? Neurologists investigated this in the CogniNMO study. A total of 17 treatment centers specialized in the disease in Germany took part. Professor Dr. Corinna Trebst and Dr. Martin Hümmert from the Department of Neurology at the Hannover Medical School (MHH) led the study. The results were published in the Multiple Sclerosis Journal.

There are a few thousand people with NMOSD in Germany. This is a rare autoimmune disease that causes relapsing inflammations of the central nervous system. Those affected suffer from limitations such as impaired vision, paralysis, incontinence and pain. “Whether their cognitive abilities are also reduced has not been clear until now. Studies had delivered different and partly contradictory results on this,” Professor Trebst says.

The function of the human brain is exceptional, driving all aspects of our thoughts and creativity. Yet the part of the human brain—the neocortex—responsible for such cognitive functions has a similar overall structure to other mammals.

Through close collaboration between The University of Queensland (UQ), The Mater Hospital and the Royal Brisbane and Women’s Hospital, researchers have discovered the human brain’s enhanced processing power may stem from differences in the structure and function of our neurons.

The results of this study have been published in Cell Reports as “High-fidelity dendritic sodium spike generation in human layer 2/3 neocortical pyramidal neurons.”

In parallel to recent developments in machine learning like GPT-4, a group of scientists has recently proposed the use of neural tissue itself, carefully grown to recreate the structures of the animal brain, as a computational substrate. After all, if AI is inspired by neurological systems, what better medium to do computing than an actual neurological system? Gathering developments from the fields of computer science, electrical engineering, neurobiology, electrophysiology, and pharmacology, the authors propose a new research initiative they call “organoid intelligence.”

OI is a collective effort to promote the use of brain organoids —tiny spherical masses of brain tissue grown from stem cells—for computation, drug research and as a model to study at a small scale how a complete brain may function. In other words, organoids provide an opportunity to better understand the brain, and OI aims to use that knowledge to develop neurobiological computational systems that learn from less data and with less energy than silicon hardware.

The development of organoids has been made possible by two bioengineering breakthroughs: induced pluripotent stem cells and 3D cell culturing techniques.

Biodegradable devices that generate energy from the same effect behind most static electricity could help power transient electronic implants that dissolve in the body, researchers say.

Implantable electronic devices now help treat everything from damaged hearts to traumatic brain injuries. For example, pacemakers can help keep hearts beating properly, while brain sensors can monitor patients for potentially dangerous swelling in the brain.

However, when standard electronic implants run out of power, they need to be removed lest they eventually become sites of infection. But their surgical removal can result in potentially dangerous complications. Scientists are developing transient implantable electronics that dissolve once they are no longer needed, but these mostly rely on external sources of power, limiting their applications.

A study published in the journal Stem Cell Reports on March 23, led by Dr. Ryosuke Tsuchimochi and Professor Jun Takahashi, examined the effects of combining cell transplantation and gene therapy for axonal outgrowth in the central nervous system. The authors demonstrated the potential of this combinatorial therapy for promoting axonal regeneration in patients with central nervous system injuries.

Stroke and traumatic brain/spinal cord injuries often damage the corticospinal tract (CST), composed of descending axonal tracts from the motor cortex down the spinal cord, that innervates motor neurons to activate skeletal muscles for controlling voluntary movements. Pharmacological and surgical interventions, in conjunction with rehabilitation, can maintain some lost motor functions, but patients with such acute neural injuries often suffer from lifelong severe motor impairment.

Cell replacement therapy—the implantation of new neurons into damaged brain regions —is viewed as a last hope that could help patients recover sufficient motor functions to live a normal life. The research team previously demonstrated that brain tissues transplanted into injured mouse brains could find their way to the CST and spinal cord but believed that further optimization of the host environment was necessary to promote CST reconstruction and functional recovery.