neuroinflammation

MS Australia awards incubator grants to four research projects

Four researchers working in multiple sclerosis (MS) were awarded incubator grants in MS Australia’s latest funding round, which they’ll use to kickstart projects designed to better understand the progressive neurodegenerative disease. Worth a total of AU$92,565, or roughly $60,000, this round of incubator grants provides seed funding…

T-cells in Bone Marrow Work to Drive Inflammatory MS Attacks

Unusual growth in an immune cell class called myeloid cells is evident in the bone marrow of people with multiple sclerosis (MS), and these cells likely contribute to the inflammation that drives the disease, according to a new study. Experiments in mice suggest that myelin-reactive T-cells can migrate to the bone…

Cancer Therapy Topotecan Could Be Repurposed to Treat MS: Study

A medication currently approved to treat certain kinds of cancer, called topotecan, could be repurposed for treating neuroinflammatory conditions such as multiple sclerosis (MS) because it reduces the inflammatory activity of immune cells called microglia. That’s according to the study, “Myeloid cell-specific topoisomerase 1 inhibition using DNA origami…

Bryostatin-1, Molecule to Protect Synapses, May Move Into MS Trials

  Synaptogenix announced plans to advance bryostatin-1, its lead candidate, into clinical trials for multiple sclerosis (MS), marking the third neurological disease the small molecule therapy is being developed to potentially treat. “Multiple sclerosis joins Alzheimer’s disease (“AD”) and Fragile X syndrome as our third indication with potential clinical…

BMS, Dragonfly Working on Immune System-targeting Therapies for MS

Dragonfly Therapeutics and Bristol Myers Squibb (BMS) announced an expanded partnership focused on discovering and developing treatment candidates for multiple sclerosis (MS) and neuroinflammation targets. The companies have been working together in therapy research and development for cancer and autoimmune diseases using Dragonfly’s proprietary immunotherapy targeting platform.

NurOwn May Curb Damaging Neuroinflammation in MS, Study Finds

NurOwn, believed to have neuroprotective and repairing effects, may also be able to curb the damaging immune responses that contribute to multiple sclerosis (MS) progression, a recent study found. This newly identified potential may extend the benefits of this cell-based therapy, its researchers believe. The findings were to be presented…

Increase in Blood-Brain Barrier Protein May Protect Against MS, Study Finds

One way the body may protect itself from nerve cell inflammation is to have cells in the blood-brain barrier increase their production of a protein that keeps immune cells from entering the brain, researchers in Germany and Canada report. The finding suggests that scientists could develop a multiple sclerosis therapy around the protein, known as EGFL7. It would work by preventing as many inflammation-generating immune cells from entering the brain. The underlying trigger for MS is immune cells crossing the blood-brain barrier to invade the central nervous system (CNS). The barrier is a selective membrane that shields the CNS from general blood circulation. Therapies that prevent immune cells from entering the brain can help control the disease, studies have shown. They include Tysabri (natalizumab, marketed by Biogen). But “as with other highly effective disease-modifying therapies which influence a broad range of peripheral immune cells, potential devastating adverse events limit the use of this therapy as a first-line agent,” the researchers wrote. The team at Mainz University Medical Center in Germany and the University of Montreal wondered if epidermal growth factor-like protein 7 (EGFL7) could prevent the brain inflammation in MS.  Although scientists had not previously linked it to MS, it was shown to regulate the migration of immune cells into breast cancer tumors. The CNS response to the chronic inflammation seen in MS patients and a mouse model of the disease was to increase EGFL7 in the blood-brain barrier, the researchers found. Researchers said the increase prevented pro-inflammatory immune cells from crossing into the CNS. Endothelial cells that line blood capillaries in the blood-brain barrier are the ones that secrete EGFL7. “We postulate that EGFL7 upregulation by BBB-ECs [brain blood barrier-endothelial cells] is induced as a compensatory mechanism to promote survival and recovery of BBB function in neuroinflammatory conditions,” the team wrote. Researchers then tested what happened in mice that lacked EGFL7. They found that the mice developed MS earlier and that their blood-brain barrier membrane was less efficient at keeping immune cells out. Treatment with EGFL7 improved the disease severity in the MS mice and tightened the blood-brain barrier, they said. “In light of our findings, smaller EGFL7 agonists, in development for other diseases, could therefore constitute an appealing therapeutic avenue for MS,” the team concluded.

Two Studies Show IL-35 Protein’s Potential to Curb Inflammation in Autoimmune Diseases

An immune signaling protein called interleukin-35 has anti-inflammatory properties that scientists might harness to develop a therapy for multiple sclerosis and other autoimmune disorders, according to two studies. Researchers at the National Eye Institute of the National Institutes of Health discovered that a subunit of interleukin 35, which is also known as IL-35, significantly reduced inflammation in mouse models of eye inflammation and multiple sclerosis. Immune B-cells produce IL-35 to communicate with, and regulate the behavior of, surrounding cells. In a previous study, the research team found that the protein could inhibit inflammation in the eyes of animals with autoimmune uveitis, or inflammation of the inner layers of the eye. An autoimmune disease is one in which the immune system attacks healthy cells instead of invaders. A drawback of trying to use a synthetic version of IL-35 as a therapy is that it's difficult to produce because of its complex structure and it's unstable in a solution. Natural IL-35 is composed of two subunits, IL-12p35 and Ebi3, which bind to create the full protein. The team wondered if they could use a subunit, instead of the full protein, as an anti-inflammatory agent. Their study, “IL-12p35 induces expansion of IL-10 and IL-35-expressing regulatory B cells and ameliorates autoimmune disease,” was published in the journal Nature Communications, They demonstrated that the IL-12p35 subunit could generate anti-inflammatory effects similar to those of the full IL-35 protein. Giving IL-12p35 to mice with uveitis promoted the expansion of immune B-cells that counteract autoimmune responses, reversing the animals' eye symptoms. In the second study, researchers discovered that the subunit tempered inflammation in a mouse model of multiple sclerosis. Giving the animals IL-12p35 every other day for up to 12 days promoted immune cell proliferation that inhibited inflammation in the mice's brains and spinal cords, improving their symptoms. The research demonstrated IL-35 and its subunit's potential to treat nerve-inflammation disorders. The team published its findings in the journal Frontiers of Immunology. The article is titled “IL-12p35 inhibits neuroinflammation and ameliorates autoimmune encephalomyelitis.” The team is now looking at IL-12p35's ability to treat other degenerative eye diseases, such as diabetic retinopathy and macular degeneration.