UCSD study says the therapy increased expression of a neuroprotective protein to help preserve brain functions, despite the presence of a destructive protein linked to ALS and Alzheimer’s
When the intestinal lining breaks down, harmful gut bacterial antigens can slip into the bloodstream alongside nutrients. This breach in the gut’s protective barrier, known as “leaky gut,” is more than a digestive issue—it’s a sign of inflammatory bowel disease (IBD) and has been increasingly linked to a number of chronic conditions.
A team of researchers working in the lab of UNLV cellular biologist Prasun Guha has uncovered a key mechanism underlying leaky gut and identified a promising and natural way to repair it. And a potential solution is already in many of the foods we eat every day.
In a study published in the journal Nature Communications, the team shares how phytic acid (or InsP6), a natural compound found in whole grains, beans, lentils, nuts, and seeds, plays an important role in maintaining the integrity of the intestinal barrier.
A group of researchers at the Medical University of South Carolina (MUSC) has recently developed a new stem cell therapy with a remarkable ability to reverse new-onset type 1 diabetes (T1D) in a mouse model of the disease. The work is published in the journal Molecular Therapy.
Hongjun Wang, Ph.D., associate director of the South Carolina Clinical & Translational Research (SCTR) Institute Pilot Program and co-scientific director for the Center for Cellular Therapy, led the team. Co-first authors Hua Wei, Ph.D.; Judong Kim, Ph.D.; and Wenyu Gou, Ph.D., together with other collaborators, conducted most of the work to establish these findings.
This research study marks a pivotal move away from the current standard of managing blood sugar through multiple daily insulin injections and toward a lasting way to reprogram the immune system itself. For the millions of people currently living with T1D, this could be a game-changer.
While many American adults are trying to reduce cholesterol levels, certain cancerous tumors have a relentless appetite for the metabolite. Some tumor cells use as much cholesterol as they can access to accelerate their growth beyond the capabilities of normal cells.
Turning tumors’ cholesterol cravings into weakness Scientists at Sanford Burnham Prebys Medical Discovery Institute and their collaborators at the University of Illinois Chicago have published findings in Science Advances regarding a potential method for turning the tables on these tumors by subverting their cholesterol cravings. The researchers revealed new insights into enzymes that help move cholesterol around cells. Without the help of these enzymes, a cholesterol traffic jam occurs, blocking the cancer cell’s ability to fuel tumor growth.
Cancer cells with a mutation in the tumor-suppressing TP53 gene are known to produce extra cholesterol. This may make them more vulnerable to starvation if scientists can put a stop to the steady supply of the lipid.
Antibodies directed against β-amyloid (Aβ) have been developed for the treatment of Alzheimer’s disease (AD). However, the in vivo central efficacy is reduced by the poor penetration of antibodies across the blood–brain barrier (BBB). In addition, these antibodies have been associated with adverse effects like amyloid-related imaging abnormalities. Thus, the development of new antibody-based therapies for AD with improved transport across the BBB may improve efficacy and reduce adverse effects. Antibodies targeting the BBB transferrin receptor (TfR) are able to cross the BBB through receptor-mediated transcytosis, producing a global distribution throughout the brain.
New research shows that specific types of brain cells become active after brain injuries and exhibit properties similar to those of neural stem cells. Astrocyte plasticity might correlate with the upregulation of the Galectin 3 protein, which may significantly contribute to discovery of additional biomarkers. The study discovered that a specific protein regulates these cells and could be a target for therapy and contribute to development of better treatments options for brain injuries. The loss of neurons, which subsequently causes impairment of brain function, is caused by the onset and progression of neurological disorders, like strokes, spinal cord injuries and neurodegenerative diseases such as Parkinson’s, Alzheimers / Dementia, ALS and MND. Effective treatment options still need to be improved. However, preclinical research has shown a promising response involving reactive astrocytes, a specific type of glial cell, which is a crucial part of the nervous system alongside neurons. Microglia and Glial cells are regarded as a safeguard for neurons, demonstrating the ability to resume cell proliferation, a mechanism essential for protecting the injury-affected brain from invasion by immune cells.[1]
Differentiation of Mesenchymal Stem Cells to Neuroglia.
Given the importance of astrocyte proliferation, these findings are relevant for understanding how changes in cerebrospinal fluid composition (upregulation of Galectin 3 protein) support the maintenance of astrocyte plasticity in the brain. Identifying Galectin 3 protein as an inducer of astrocyte plasticity has helped discover other biomarkers that offer beneficial modulation inside the injured brain parenchyma. These regulators of astrocyte proliferation after acute injury offer great promise for the future clinical applications of these biomarkers as indicators for detecting a beneficial reaction of glial stem cell therapy or help identify the presence of other cells with stemness potential in an injured patient’s brain [5].
For millions of people living with osteoarthritis, daily life can involve a frustrating cycle of pain and stiffness. While current treatments like over-the-counter medications or steroid injections can temporarily dull the ache, they do not stop the joint from deteriorating. A Yale study published in the journal Bioactive Materials found that the medication lacosamide acts as a highly effective, dual-purpose treatment that relieves joint pain and reverses cartilage damage in osteoarthritis, especially when a specialized hydrogel delivers the drug directly into the joint.
Large vestibular schwannomas (VS) often compress the brainstem and differ in their relation to the internal auditory canal (IAC); the significance of these radiographic features on postoperative outcomes remains unclear. This study quantifies the impact of brainstem compression (BSC) and position relative to the IAC on surgical outcomes in VS.
We retrospectively identified 116 patients with sporadic unilateral VS ≥ 3 centimeters (2017–2022). Neurofibromatosis 2 cases were excluded. BSC was quantified with MRI T1 post-contrast axial images as the perpendicular distance from the brainstem-cerebellum to the point of maximal compression. Anterior and posterior IAC extension were measured relative to a line bisecting the IAC from the porus to fundus. Outcomes included postoperative facial nerve (FN) function, extent of resection (EOR), and length of stay (LOS).
Greater anterior extension was associated with decreased EOR in univariate analysis (OR = 1.12, p = 0.03), but not after controlling for tumor size and age (OR = 1.09, p = 0.158). Greater BSC was associated with worse FN function at 2–3 weeks postoperatively on univariate (OR = 1.08, p = 0.036) and approached significance on multivariate analysis (OR = 1.07, p = 0.08). Posterior extension was associated with increased LOS in univariate (β = 217.57 min, p = 0.024), but not multivariate analysis. Neither anterior extension nor BSC were associated with LOS. Older age correlated with a lower rate of GTR and longer LOS in multivariate analysis (EOR: OR = 1.05, p = 0.003; LOS: β = 79.84 min, p = 0.026).