Stream Neuroscience’s Post

How an Endocannabinoid can save your brain: "Traumatic brain injury triggers the accumulation of harmful mediators that may lead to secondary damage. Protective mechanisms to attenuate damage are also set in motion. 2-Arachidonoyl glycerol (2-AG) is an endogenous cannabinoid identified both in the periphery and brain; its physiological roles have only partially clarified. Research shows that after injury to the mouse brain, 2-AG may have a neuroprotective role involving the cannabinoid system. After a closed head injury (CHI) in mice, the level of endogenous 2-AG was significantly elevated. Researchers administered synthetic 2-AG to mice after CHI and found a significant reduction of brain edema, better clinical recovery, reduced infarct volume, and reduced hippocampal cell death compared with controls. Functional recovery was significantly enhanced when 2-AG was administered with additional inactive 2-acyl-glycerols usually present in the brain." Cannabis saves lives. -Mike Robinson, Founder Nanobles Corp. / Global Cannabinoid Research Center (GCRC)

In the past decade, there has been increased focus on glial cells in relation to neurological disorders. As a result, we conducted a review on the use of glial cells with three-dimensional scaffolds and discovered that suitable scaffolds, such as self-assembling peptides, could inhibit inflammatory responses by altering glial polarization. You can access the full-text article using the link below: https://lnkd.in/dQtwK5F5.

Excited to share our new publication on accelerated continuous theta burst stimulation for bipolar depression. The RCT was conducted from 2018 to 2020 @Zorggroep UPC Duffel, but more recently, we measured plasma metabolites of the kynurenine pathway and found that higher baseline quinolinic acid levels predicted better treatment outcome. This finding is particularly intriguing, as quinolinic acid acts centrally as an NMDA receptor agonist. These results contribute to the growing interest in the role of the glutamate system in the brain's neuroplastic potential. Could pre-treatment normalization of quinolinic acid levels, or pharmacologically mimicking its effects, increase remission rates? Let's find out! (Note: The treatment protocol from this trial could use some optimization tweaks using recent developments in the field;)) https://lnkd.in/egQVvCHq

The role of kynurenine metabolites in the prediction of TMS outcome in bipolar disorder? Find out more in our published manuscript in Journal of Affective Disorders!

SOVATELTIDE AKA #TYVALZI A highly selective endothelin-B receptor agonist and synthetic analog of endothelin-1, is being developed as a neural progenitor cell therapeutic agent for the treatment of acute cerebral ischemic stroke (ACIS), hypoxic-ischemic encephalopathy (HIE), spinal cord injuries and Alzheimer's disease. Neurological/neurovascular disorders constitute the leading cause of disability and the second leading cause of death globally. In May 2023, sovateltide was approved in India for the treatment of cerebral ischemic stroke within 24 hr of stroke onset. Dose: 0.3 mcg/kg of body weight/dose Total doses: 9 Doses (Three doses on each of day 1, day 3, and day 6) Dosing interval: 3 Hours First dose: Within 24 hours of the onset of the stroke Method of administration: Reconstitute 30mcg Tyvalzi in 5 ml of Sodium chloride injection IP (0.9% w/v). Gently swirl to dissolve the content. The reconstituted Tyvalzi should be withdrawn in a sterile disposable syringe at a dose of 0.3 ug/kg of body weight and administered intravenously over one minute. The reconstituted volume withdrawn from the vial is adjusted according to the body weight. Directions for proper use of Tyvalzi a) Use an aseptic technique for the reconstitution. b) Do not store or refrigerate the reconstituted drug; use it immediately. c) Do not use it if the flip-off aluminum seal is found broken or tampered. #neuro #stroke #tyvalzi #clinicalpharmacist

Exiting news today: “NLS Pharmaceutics Announces Promising Preclinical Data for First-in-Class Non-Sulfonamide, Dual Orexin Receptor Agonists for the Potential Treatment of Narcolepsy and Neurological Disorders” https://lnkd.in/eBE7pY-m

Insulin restores retinal ganglion cell functional connectivity and promotes visual recovery in glaucoma Science Advances https://lnkd.in/gJs6cBN7

Vitamin B6 is essential for brain function, and its deficiency is linked to cognitive impairments. Recent research identifies 7,8-dihydroxyflavone (7,8-DHF) as a potent inhibitor of PDXP, an enzyme that regulates the active form of vitamin B6. This discovery offers new insights into therapeutic strategies for brain disorders associated with vitamin B6 deficiency. Read the full paper here: https://lnkd.in/e6qb6JU6

NEW PLATFORM OVERCOMES BLOOD-BRAIN BARRIER FOR DRUG DELIVERY Researchers have developed a breakthrough system to deliver large therapeutic molecules into the brain, overcoming the challenges of the blood-brain barrier. The innovative blood-brain barrier-crossing conjugate (BCC) platform utilizes a biological process called γ-secretase-mediated transcytosis to safely transport drugs like oligonucleotides and proteins into the central nervous system via intravenous injection. In mouse models and human brain tissue, the system effectively silenced harmful genes linked to diseases such as ALS and Alzheimer’s without causing significant side effects. This advancement could revolutionize treatments for neurological and psychiatric disorders, solving a critical challenge in brain research. Key Facts: 1. The BCC system uses γ-secretase-mediated transcytosis to bypass the blood-brain barrier. 2. It successfully delivered drugs targeting harmful genes in ALS and Alzheimer’s disease. 3. The treatment was well-tolerated and effective in both mouse models and human brain tissue. Source: https://lnkd.in/gjyf7_Pb

Altering pro-inflammatory glial responses to effectively illuminate neuroprotective mechanisms via targeting the GR (glucocorticoid receptor) to impede PD neuropathology. It is commonly understood in the realm of balance and movement disorders, that these receptors (GR) are implicated in the neuropathology of PD, and typically also serve to modulate numerous neuroinflammatory signaling pathways in the brain. As current treatments for PD largely center around dopamine replacement therapies (failing to prevent the condition's progression), underscoring the need for neuroprotective interventions via altering pro-inflammatory glial responses is a real breakthrough.  The inflammatory response to neuronal injury being responsible for most of the dopamine neuron loss (w/a marked reduction in measures of cellular inflammation correlated with preservation of the number of dopamine neurons). This therapeutic (PT150) -- shifting microgliosis in the nigrostriatal pathway -- to promote a potentially neuroprotective activity is very promising and suggests this orally bioavailable drug could be neuroprotective in disease-modifying PD.