All articles tagged with #blood brain barrier
Researchers report that a vitamin B12–based compound, nitrosylcobalamin (NO-Cbl), can cross the blood-brain barrier, selectively accumulate in glioblastoma tumors, and deliver nitric oxide to cancer cells in preclinical models; it also shows synergistic activity with temozolomide (and TRAIL) to enhance tumor suppression, offering a promising but early approach that requires further validation before clinical use.
Monash University researchers report in ACS Chemical Neuroscience that the copper compound Cu(ATSM) strengthens the brain's waste-clearing system by boosting P-glycoprotein pumps at the blood-brain barrier in an Alzheimer's model, reducing amyloid-beta by 42% and improving spatial memory by about 44% over 56 days, pointing to a therapy for neurovascular dysfunction; Cu(ATSM) has safety data from other neurological conditions, potentially speeding human testing, though exact clearance pathways and microglial involvement require further study.
Monash University researchers used Cu(ATSM), a copper-delivery compound, to repair the brain’s blood–brain barrier by increasing the P-glycoprotein clearance pumps, which reduced toxic amyloid-beta by about 42% and improved long-term spatial memory by roughly 44% in an APP/PS1 mouse model over 56 days, suggesting copper-based biometal therapy could be a promising route for early symptomatic Alzheimer's disease with potential for quicker human testing due to prior safety evaluations; future work aims to map the precise clearance mechanisms and pathways.
Researchers used supramolecular nanoparticles that act as drugs to repair the brain's blood-brain barrier and restart its waste-clearance system. In mice with high amyloid-β, three injections reduced brain Aβ by 50–60% within an hour, with months-long vascular and cognitive improvements; the approach leverages the LRP1 transport system to reset clearance. While promising, the work is in animal studies and human trials remain years away.
Lab findings and observational studies suggest erythritol could damage the blood-brain barrier and disrupt vascular control, potentially increasing stroke and cardiovascular risk, but results are preliminary (cell-based and population data) and require further validation; regulators still deem erythritol safe for now.
MIT researchers reveal a laser that self-organizes into a stable pencil beam inside a multimode fiber under precise on-axis high-power conditions, enabling ultrafast, high-resolution 3D imaging of the blood–brain barrier and real-time tracking of drug uptake without fluorescent tags—potentially speeding brain-targeted therapy research by about 25x and opening paths to imaging neurons and other tissues.
A UCSF study in mice shows exercise increases GPLD1 in the blood, which helps prune TNAP in brain blood vessels, strengthening the blood-brain barrier, reducing inflammation, and lowering amyloid beta clumps associated with Alzheimer's. The findings suggest a body-brain mechanism behind exercise’s cognitive benefits and point to potential therapies that mimic GPLD1, though human relevance remains to be confirmed.
Specialized brain cells called tanycytes clear tau proteins from cerebrospinal fluid into the bloodstream, helping remove potentially toxic tau from the brain. In Alzheimer's disease, tanycytes are damaged and less tau moves to the blood, correlating with brain tau buildup; this reveals a potential mechanism for disease progression and a new target to boost tau clearance.
UC San Francisco researchers show that exercise increases the liver enzyme GPLD1, which travels to brain blood vessels and removes TNAP from the blood-brain barrier. This restores barrier integrity and reduces leakiness and inflammation in aging mice, helping memory and cognitive performance, and suggesting new therapeutic avenues for aging and Alzheimer’s-related decline.
New lab and observational evidence suggests the sugar substitute erythritol can damage cells of the blood-brain barrier, trigger oxidative stress, and lower nitric oxide while raising endothelin-1, potentially narrowing cerebral vessels and hindering clot dissolution—factors that could elevate stroke risk; these findings align with studies linking erythritol to higher cardiovascular events, though most experiments used isolated cells and require validation in more realistic models.
Aerska, a Dublin/London biotech, raised $39 million in a second financing round to advance brain-shuttle delivery of siRNA that silences disease-causing brain genes, leveraging an iron-molecule–like carrier to cross the blood-brain barrier.
Researchers tested IKVAV-PA, a peptide-based nanomaterial, in a mouse model of acute ischemic stroke and found that systemic delivery allows the molecules to cross the blood-brain barrier and reduce brain tissue damage, inflammation, and harmful immune responses after reperfusion, indicating potential as an adjunct therapy—though human safety and long-term efficacy remain to be studied.
A Cell study (15 years in the making) finds that a protein called cystatin C, produced by cancer cells, can cross the blood–brain barrier and help break apart amyloid plaques in mouse models of Alzheimer’s disease, offering a possible explanation for the observed link between cancer and lower Alzheimer’s risk and suggesting a new avenue for drug development—though the findings are preclinical and in animals.
Northwestern researchers developed an intravenously delivered supramolecular peptide therapy, IKVAV-PA, that crosses the blood-brain barrier after a stroke, accumulates at injury sites, and reduces tissue damage and inflammation in mice with a single post-reperfusion dose, without detectable organ toxicity. While no short-term behavioral improvement was seen, the approach shows promise as an adjunct to clot-reopening treatments and could extend to other brain injuries pending longer-term studies on cognitive and functional recovery.
Northwestern researchers have developed an injectable regenerative nanomaterial built from dynamic “dancing molecules” that can cross the blood-brain barrier after reperfusion in a mouse model of ischemic stroke. Delivered intravenously immediately after clot removal, the therapy reduced brain damage and inflammation without observed toxicity, suggesting it could complement clot-busting treatments. The approach relies on smaller peptide assemblies crossing the BBB before larger nanofibers form in brain tissue, and may have implications for traumatic brain injury and neurodegenerative diseases. Next steps include longer-term functional studies and exploring additional regenerative signals.