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Glioblastoma (GBM) is a highly aggressive and malignant brain tumor with a poor prognosis. Treatment options are limited, and the development of effective therapeutics is a major challenge. Here are some current and emerging therapeutic strategies for GBM:

Current Therapies 1. Surgery: Surgical resection is the primary treatment for GBM, aiming to remove as much of the tumor as possible. 2. Radiation Therapy: Radiation therapy is used to kill remaining tumor cells after surgery. 3. Temozolomide (TMZ): TMZ is a chemotherapy drug that is used to treat GBM, often in combination with radiation therapy. 4. Bevacizumab (Avastin): Bevacizumab is a monoclonal antibody that targets vascular endothelial growth factor (VEGF) to inhibit angiogenesis.

Emerging Therapies 1. Immunotherapy: Immunotherapies, such as checkpoint inhibitors (e.g., PD-1/PD-L1 inhibitors) and cancer vaccines, aim to stimulate the immune system to attack GBM cells. 2. Targeted Therapies: Targeted therapies focus on specific molecular pathways involved in GBM, such as the PI3K/AKT/mTOR pathway. 3. Gene Therapy: Gene therapies aim to introduce genes that can help kill GBM cells or inhibit tumor growth. 4. Oncolytic Viruses: Oncolytic viruses are engineered to selectively infect and kill GBM cells. 5. CAR-T Cell Therapy: CAR-T cell therapy involves genetically modifying T cells to recognize and attack GBM cells. 6. Small Molecule Inhibitors: Small molecule inhibitors target specific proteins involved in GBM, such as EGFR, PDGFR, and BRAF.

A study from Tübingen University and the German Center for Diabetes Research reveals that the brain plays a crucial role in obesity and type 2 diabetes development. It shows that even a brief period of consuming high-calorie processed foods can significantly alter brain insulin sensitivity, a key factor in weight gain and metabolic disorders. The research demonstrated that insulin’s appetite-suppressing effect in the brain diminishes after a short-term high-calorie diet, leading to insulin resistance. These effects were observed in healthy participants, suggesting that dietary habits could influence brain function before any significant weight gain occurs. Further research is needed to understand the brain’s role in these conditions.


The number of obese persons has grown significantly in recent decades, which presents significant difficulties for those who are impacted, healthcare systems, and those who provide treatment. The hormone insulin plays a key role in the development of obesity. Up until recently, there have been numerous signs indicating insulin causes neurodegenerative and metabolic disorders, especially in the brain. A recent study by the University Hospital of Tübingen, the German Center for Diabetes Research (DZD), and Helmholtz Munich offers intriguing new insights into the origins of type 2 diabetes and obesity as well as the brain’s function as a critical control center.

Obesity has only been officially recognized as a disease in Germany since 2020, despite the fact that it has long been known to cause a number of illnesses, including diabetes, heart attacks, and even cancer. The World Health Organization has already declared obesity to be an epidemic, affecting over one billion individuals globally and almost 16 million in Germany alone. A body mass index of 30 or more is considered obese, and a poor diet and insufficient exercise are frequently cited as the causes of this chronic illness. However, the mechanisms in the body that lead to obesity and cause the disease are more complex.

Obesity and the role of insulin in the brain

Unhealthy body fat distribution and chronic weight gain are linked to the brain’s sensitivity to insulin. What specific functions does insulin perform in the brain, and how does it affect individuals of normal weight? In their study, Prof. Dr. Stephanie Kullmann and her colleagues at the Tübingen University Hospital for Diabetology, Endocrinology, and Nephrology found the answer to this query. “Our findings demonstrate for the first time that even a brief consumption of highly processed, unhealthy foods (such as chocolate bars and potato chips) causes a significant alteration in the brain of healthy individuals, which may be the initial cause of obesity and type 2 diabetes,” says Prof. Kullmann, the study’s leader. In a healthy state, insulin has an appetite-suppressing effect in the brain. However, in people with obesity in particular, insulin no longer regulates eating behavior properly, resulting in insulin resistance.

Basically mushrooms can cure all major illnesses all over the human body and brain. If all the pharmaceutical companies got into business with Chinese medicine which has used mushrooms of all types we essentially have a no side effect system of 100 percent healing. Even the basic food pyramid has show essentially to prove beneficial to humans more than medicines. Also essentially nanotransfection for people that have lost limbs or lost any body part could in the future regenerate limbs similar to wolverine like in the marvel comics but at a slower pace but would heal anything while the mushrooms keep one well and fed. A lot of the American studies are a stop gap measure while mushrooms can cure things slowly but to 100 percent. Along with healthy eating and nanotransfection one could have all they need for any regeneration in the far future. In the future this technology and food could essentially allow for minimal down time healing inside and the foods would fuel the body. It could be put on a smartphone where even trillions of dollars would be saved getting doctor treatments down to a dollar or less for entire body scans and healing. It would be the first step towards Ironman but using the human body to heal itself and the foods to fuel regeneration.


The WHO has published the first list of priority fungal pathogens, which affect more than 300 million people and kill at least 1.5 million people every year. However, funding to control this scourge is less than 1.5% of that devoted to infectious diseases.

Researchers have mapped the long-range synaptic connections involved in vocal learning in zebra finches, uncovering new details about how the brain organizes learned vocalizations such as birdsong.

The study, published as a Reviewed Preprint in eLife, is described by the editors as having fundamental significance and compelling evidence clarifying how four distinct inputs to a specific region of the brain act on three distinct cell types to facilitate the learning and production of birdsong.

Understanding how the brain integrates sensory and motor information to guide learned vocalizations is crucial for studying both birdsong and human speech. The courtship song of male is a well-studied example of a naturally learned behavior, and is controlled by a set of interconnected forebrain regions in the dorsal ventricular ridge (DVR)—the avian equivalent of the mammalian neocortex.

I think Paul may have posted this already, if so here is some more information from a site about drug repurposng. Its really cool.

Click the video above to watch a story that ran on CBS Evening News about leucovorin for ASD.

Every Cure is excited to highlight the potential role that leucovorin (folinic acid) may play in improving verbal communication in some individuals with autism spectrum disorder (ASD) who have speech challenges and certain antibodies that cause a vitamin deficiency in the brain. As a nonprofit research organization committed to identifying and elevating potential repurposed treatments, we’ve summarized information about this promising drug repurposing opportunity below.

A vitamin deficiency may contribute to speech challenges in some individuals with ASD.

A new study published in Cell Reports reveals a breakthrough discovery linking genetic variants in the gene ITSN1 to a significantly elevated risk of Parkinson’s disease, a neurodegenerative condition that affects nearly 2% of adults older than 65 years.

These findings were subsequently validated across three independent cohorts comprising more than 8,000 cases and 400,000 controls. Importantly, ITSN1 carriers trended toward earlier age of disease onset.

ITSN1 plays an important role in how neurons send messages to each other – a process called synaptic transmission – making it particularly relevant to Parkinson’s disease, a condition in which disruption of nerve signals leads to the typical symptoms of impaired gait and balance, tremors and rigidity. “We also showed in fruit flies that reducing ITSN1 levels worsens Parkinson’s-like features, including the ability to climb. We plan to extend these investigations to stem cell and mouse models,” the author said.

Interestingly, previous studies have recently implicated similar ITSN1 mutations in autism spectrum disorder (ASD). Other emerging data also have suggested an association between ASD and Parkinson’s disease, indicating that people with ASD are three times more likely to develop parkinsonism.

The body you inhabit is made up of lots of moving parts that need to communicate with each other.

Some of this communication – in the nervous system, for example – takes the form of bioelectrical signals that propagate through the body to trigger the appropriate response.

Now, US researchers have discovered that the epithelial cells that line our skin and organs are able to signal the same way to communicate peril. They just use a long, slow ‘scream’, rather than the rapid-fire communication of neurons.

Brain implants hold immense promise for restoring function in patients with paralysis, epilepsy and other neurological disorders. But a team of researchers at Case Western Reserve University has discovered that bacteria can invade the brain after a medical device is implanted, contributing to inflammation and reducing the device’s long-term effectiveness.

The research, published in Nature Communications, could improve the long-term success of brain implants now that a target has been identified to address.

“Understanding the role of bacteria in implant performance and brain health could revolutionize how these devices are designed and maintained,” said Jeff Capadona, Case Western Reserve’s vice provost for innovation, the Donnell Institute Professor of Biomedical Engineering and senior research career scientist at the Louis Stokes Cleveland VA Medical Center.