Lifeboat Foundation

A collaborative project to bring the promise of cell therapy to patients with a deadly form of brain cancer has shown dramatic results among the first patients to receive the novel treatment. In a paper published today in The New England Journal of Medicine, researchers from the Mass General Cancer Center, a member of the Mass General Brigham healthcare system, shared the results for the first three patient cases from a phase 1 clinical trial evaluating a new approach to CAR-T therapy for glioblastoma (GBM). The trial, known as INCIPIENT, is designed to evaluate the safety of CARv3-TEAM-E T cells in patients with recurrent GBM. Just days after a single treatment, patients experienced dramatic reductions in their tumors, with one patient achieving near-complete tumor regression. In time, the researchers observed tumor progression in these patients, but given the strategy’s promising preliminary results, the team will pursue strategies to extend the durability of response.

“This is a story of bench-to-bedside therapy, with a novel cell therapy designed in the laboratories of Massachusetts General Hospital and translated for patient use within five years, to meet an urgent need,” said Bryan Choi, MD, PhD, neurosurgeon and associate director of the Center for Brain Tumor Immunology and Immunotherapy, Cellular Immunotherapy Program, Mass General Cancer Center and Department of Neurosurgery. “The CAR-T platform has revolutionized how we think about treating patients with cancer, but solid tumors like glioblastoma have remained challenging to treat because not all cancer cells are exactly alike and cells within the tumor vary. Our approach combines two forms of therapy, allowing us to treat glioblastoma in a broader, potentially more effective way.”

Diving into the complexities of Seronegative Autoimmune Encephalitis — a journey through diagnostic hurdles and treatment paths. Discover more: 👉 https://bit.ly/3TwTulh ✨

Seronegative autoimmune encephalitis (AE) is a rare, immune-mediated inflammatory syndrome that presents with a wide spectrum of neuropsychiatric symptoms, such as cognitive impairment, seizures, psychosis, focal neurological defects, and altered consciousness. This disease process presents with no identifiable autoimmune antibodies, which leads to uncertain diagnosis, delayed treatment, and prolonged hospital admissions. Early diagnosis and prompt treatment of AE should not be delayed, as early recognition and treatment leads to improved outcomes and disease reversibility for these patients. In this study, we present a case report of a 77-year-old male who presented with acutely altered mental status. This patient underwent an extensive workup and demonstrated no signs of clinical improvement throughout a prolonged hospital admission.

Traumatic brain injury (TBI) causes a high rate of mortality and disability, and its treatment is still limited. Loss of neurons in damaged area is hardly rescued by relative molecular therapies. Based on its disease characteristics, we transplanted human embryonic stem cell-(hESC-) derived cerebral organoids in the brain lesions of controlled cortical impact-(CCI-) modeled severe combined immunodeficient (SCID) mice. Grafted organoids survived and differentiated in CCI-induced lesion pools in mouse cortical tissue. Implanted cerebral organoids differentiated into various types of neuronal cells, extended long projections, and showed spontaneous action, as indicated by electromyographic activity in the grafts. Induced vascularization and reduced glial scar were also found after organoid implantation, suggesting grafting could improve local situation and promote neural repair. More importantly, the CCI mice’s spatial learning and memory improved after organoid grafting. These findings suggest that cerebral organoid implanted in lesion sites differentiates into cortical neurons, forms long projections, and reverses deficits in spatial learning and memory, a potential therapeutic avenue for TBI.

The cerebral cortex forms early in development according to a series of heritable neurodevelopmental instructions. Despite deep evolutionary conservation of the cerebral cortex and its foundational six-layered architecture, significant variations in cortical size and folding can be found across mammals, including a disproportionate expansion of the prefrontal cortex in humans. Yet our mechanistic understanding of neurodevelopmental processes is derived overwhelmingly from rodent models, which fail to capture many human-enriched features of cortical development. With the advent of pluripotent stem cells and technologies for differentiating three-dimensional cultures of neural tissue in vitro, cerebral organoids have emerged as an experimental platform that recapitulates several hallmarks of human brain development.

Genetics of human brain development.

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Brain organoids are self-organizing tissue cultures grown from patient cell-derived induced pluripotent stem cells. They form tissue structures that resemble the brain in vivo in many ways. This makes brain organoids interesting for studying both normal brain development and for the development of neurological diseases. However, organoids have been poorly studied in terms of neuronal activity, as measured by electrical signals from the cells.

A team of scientists led by Dr. Thomas Rauen from the Max Planck Institute for Molecular Biomedicine in Münster, Germany, in collaboration with Dr. Peter Jones’ group at the NMI (Natural and Medical Sciences Institute at the University of Tübingen, Germany), has now developed a novel microelectrode array system (Mesh-MEA) that not only provides optimal growth conditions for human brain organoids, but also allows non-invasive electrophysiological measurements throughout the entire growth period. This opens up new perspectives for the study of various brain diseases and the development of new therapeutic approaches.

The study is published in the journal Biosensors and Bioelectronics.

Researchers at Rutgers and Emory University are gaining insights into how schizophrenia develops by studying the strongest-known genetic risk factor.

When a small portion of chromosome 3 is missing—known as 3q29 deletion syndrome—it increases the risk for schizophrenia by about 40-fold.

Researchers have now analyzed overlapping patterns of altered gene activity in two models of 3q29 deletion syndrome, including mice where the deletion has been engineered in using CRIPSR, and human brain organoids, or three-dimensional tissue cultures used to study disease. These two systems both exhibit impaired mitochondrial function. This dysfunction can cause energy shortfalls in the brain and result in psychiatric symptoms and disorders.

Research conducted by Brown University’s Carney Institute for Brain Science illustrates how parts of the brain need to work together to focus on important information while filtering out distractions.

Imagine a busy restaurant: dishes clattering, music playing, people talking loudly over one another. It’s a wonder that anyone in that kind of environment can focus enough to have a conversation. A new study by researchers at Brown University’s Carney Institute for Brain Science provides some of the most detailed insights yet into the brain mechanisms that help people pay attention amid such distraction, as well as what’s happening when they can’t focus.

In an earlier psychology study, the researchers established that people can separately control how much they focus (by enhancing relevant information) and how much they filter (by tuning out distractions). The team’s new research, published in Nature Human Behaviour, unveils the process by which the brain coordinates these two critical functions.

Researchers from Tohoku University have created a theoretical framework for an advanced spin wave reservoir computing (RC) system that leverages spintronics. This innovation advances the field toward realizing energy-efficient, nanoscale computing with unparalleled computational power.

Details of their findings were published in npj Spintronics on March 1, 2024.