An unexpected lab observation has led a team of scientists to discover how diet can influence survival in animal models of glioma, one of the most aggressive and deadly forms of brain cancer. Researchers at Baylor College of Medicine, the Duncan Neurological Research Institute (Duncan NRI) at Texas Children’s Hospital and collaborating institutions report in the Proceedings of the National Academy of Sciences how limiting a single nutrient, the amino acid methionine, in the diet destabilized DNA organization and led to cancer cell death and increased animal survival. These findings open new possibilities for treating one of the most challenging forms of brain cancer.

“Cancer cells, including gliomas, often depend on methionine. Methionine is an essential amino acid, meaning that the body does not produce it on its own; it must be consumed in the diet. Glioma cells are unusually dependent on methionine to fuel rapid growth and control gene activity,” said corresponding author Dr. Benjamin Deneen, professor and Dr. Russell J. and Marian K. Blattner Chair in the Department of Neurosurgery and director of the Center for Cancer Neuroscience, all at Baylor.

“In the current study, we wanted to know, if tumors depend so much on methionine, what happens if we reduce the supply?” said first author Brittney Lozzi, a graduate student in the Deneen lab.

Cocaine can speedily rewire high-level brain circuits that support learning, memory and decision-making, according to new research from UC Berkeley and UCSF. The findings shed new light on the frontal brain’s role in drug-seeking behavior and may be key to tackling addiction.

She had not spoken a full sentence in five years. Then she took a single 5 gram dose of psilocybin (which is a very large dose). She slept 19 hours. When she woke up, she spoke for hours about her life. She recognized family and held real conversations. She regained bladder control after five years, and walked on her own. She dressed herself. These gains continued for weeks.

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Background:

Advanced Alzheimer’s disease (AD) is generally regarded as a stage of irreversible functional decline. Psilocybin is known to transiently alter large-scale brain network dynamics and to induce plasticity-related mechanisms in preclinical models, yet clinical data in advanced dementia remain lacking.

Case presentation:

We report the case of an octogenarian Japanese-American woman with a 10-year history of Alzheimer’s disease, including 5 years of marked hypofunction and predominantly monosyllabic speech. Baseline features included chronic urinary incontinence, executive dysfunction, dysphagia, dependent mobility, flat affect, and severe reduction in spontaneous communication. The patient received 5 g of orally administered psilocybin-containing mushrooms (Enigma strain). The acute phase was marked by autonomic activation, clinically suspected hyperthermia, profuse sweating, and a prolonged deep sleep-like state. Approximately 19 h post-administration, spontaneous autobiographical speech emerged.

At age 49, Jan Janisch-Hanzlik’s multiple sclerosis was destroying her freedom to live the life she wanted. She gave up her active nursing job for a desk role. Frequent falls made her afraid to carry her grandchildren. She had to move to a bigger house to make room for the wheelchair she feared she might end up needing full-time.

Even the best available medication wasn’t improving Janisch-Hanzlik’s symptoms, and she worried they’d only get worse. So when she learned about a trial of CAR T cell therapy at the University of Nebraska Medical Center in Omaha, close to the city of Blair where she lives, she phoned the clinic every other month until they were ready to enroll her as the first patient.

Originally designed to target and wipe out cancer by reprogramming the patient’s immune cells, CAR T is now being offered to patients in hundreds of clinical trials for autoimmune conditions like multiple sclerosis, lupus, Graves’ disease, vasculitis and many others. The hope is that CAR T can duplicate the success it has demonstrated in a range of blood cancers by hunting down and eliminating cells that target the self in autoimmune diseases. This would essentially reset the body’s defenses to a state like the one that existed before the disease took hold.

New research from the Mark and Mary Stevens Neuroimaging and Informatics Institute (Stevens INI) at the Keck School of Medicine of USC has discovered subtle but widespread differences in the brain’s communication networks in people with bipolar disorder, offering new insight into how illness severity and treatment may relate to brain wiring.

Published in Biological Psychiatry, the study was led by Leila Nabulsi, Ph.D., a senior research associate at the Stevens INI, together with Dara M. Cannon, Ph.D., professor at the University of Galway, Ireland. The team analyzed brain scans from 449 people with bipolar disorder and 510 healthy controls across 16 international research sites through the ENIGMA Bipolar Disorder Working Group.

This work was made possible by ENIGMA, an international consortium founded and led in part by Paul M. Thompson, Ph.D., associate director of the Stevens INI. ENIGMA brings together researchers worldwide to pool their brain imaging and clinical data, allowing them to detect subtle patterns that would be difficult to identify in smaller studies.

Researchers created Compound 10 to block GRK2 enzyme aggregation and protect mitochondria in Alzheimer’s disease.