Neuroprotection - Science topic
“Neuroprotection” is a widely explored treatment option for many central nervous system (CNS) disorders including neurodegenerative diseases, stroke, traumatic brain injury, and spinal cord injury. Neuroprotection aims to prevent or slow disease progression and secondary injuries by halting or at least slowing the loss of neurons.
Questions related to Neuroprotection
I want to study the neuroprotection of ghrelin in mice neurological disease model, but there is differences in this drug between human and rat, which one i should choose since both type of drug has been used in the published paper. Thanks.
Magnesium Sulphate is administered to pregnant women during preterm labour for fetal neuroprotection. Would like to know about any studies which have been done to evaluate its beneficial effects during early neonatal period.
MgSO4 is usually administered during preterm labour for neuroprotection. I would like to know whether there are any beneficial effects during early neonatal period also.
I have been working on a TBI mouse model and looking at AQP4. The literature provided by abcam shows the western blot data to have a band at 46 kDa and another one at 20kDa that they cannot identify. My blots have a double band at 48 and 46 kDa and a large band at 20 kDa. Does anyone have any experience working with this antibody? Any suggestions or ideas about what these bands represent?
I am working on estradiol neuroprotection impact and measuring its concentration in hippocampal female rats in their diestrus phase by 17beta-Estradiol ELISA (Diagnostics Biochem Canada). To extract estradiol from hippocampus the tissue was homogenized in 150µl PBS and centrifuged at 15,000g for 30 min at 4ºC and supernatants were collected. The problem is almost no level of estradiol was detected through this method.
We would like to roughtly assess the potential neuroprotective ability of a certain agent to prevent people from developing Parkinson's disease (PD). PD has an incidence of 1% in the general population over 60 years. We are planning to conduct a retrospective study on a group of people, who have all been exposed to this agent for many years. The potential beneficial effect of the agent would also consider information about time of exposure to the agent and the estimated total received dosage of the agent during the lifespan. In case if the agent has neuroprotective properties, we predict people who were exposed to it for a longer period at higher dosages have lower overall prevalence of PD than the general population of the same age group. Our concern is - what would be a minimum number of participants who are 60 years old or older, to be able to estimate the agent's potential beneficial effect?
My lab is studying neuroprotective effect towward Sh-SY5Y cells. However, when I seed the Sh-Sy5Y cells in Sigma 96 well plate coated with PDL (cls3842), 3 days later, all Sh-SY5Y cells clumped together forming small lumps. In normal, they should be divided indivudally, equally spread inside the wells. This abnormal phenomenon does not appear when we used in a 96 well plate without PDL.
It surprises me since I read papers that using SH-SY5Y cells coated with PDL before.
I am wondering have you heard of any similar observation, and do you have any suggestion to prevent this?
Or do you guys have any suggestion for how to do pdl toward plates?
i will do my research which is testing neuroprotection of drug onglobal cereberal ischemia reperfusion model in wistar rat but i want to know the factor should i considered when i choose age and weight of the rat
Hi Everyone. I am trying to check the neuroprotective activity of some compounds in the rotenone model of Parkinson's disease in PC-12, for which I will check the effect of that compound on cell viability first. I want to ask whether it is required to differentiate PC-12 for this purpose, as I tried to differentiate the cells using 30 ng/mL as well as 50 ng/mL NGF. I am able to see the differentiated cells in 3-4 days in 96 well plate, but NGF itself is causing cell death, which could be a variable for the cell viability test.
I am a nurse who is researching why some cancer patients are not reporting the same dramatic effectiveness of high-dose cannabinoid extracts on causing tumor regression as some others. Here is the best current article I know of which explains the Anticancer Mechanisms of Cannabinoids and includes the information about THC-resistant glioma cells that overexpressed Midkine (MDK) and became sensitive to the THC after pharmacologic ALK inhibition. Velasco G, Sánchez C, Guzmán M. Anticancer mechanisms of cannabinoids. Current Oncology. 2016;23(Suppl 2):S23-S32. doi:10.3747/co.23.3080. https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4791144/
We know there are different rates of over-expression of CB1 and CB2 which appear to play at least a partial role but, of course, the various tumor microenvironment factors, mutations and, especially, this information about MDK/ALK as a mechanism of resistance to THC should soon produce much more clarity about this problem.
I am intrigued by the knowledge that Non-Small-Cell Lung Cancer and many Breast Cancers often have ALK mutation (and there are significant patients with NSLC and Breast Cancer who do not seem to get as much/any tumor regression yet others get dramatic regression and even No Evidence of Disease with high-doses of THC and CBD). The NSLC patients with ALK mutations are suddenly becoming more treatable after addition of an ALK inhibitor crizotinib, ceritinib, alectinib and others. I have been unable to find any research assessing ALK mutation status and THC resistance or sensitivity for tumors from other tissues than the brain.
I can't help but wonder if research could show if there are THC-resistant tumors of lung and breast ++ that are also ALK mutated or Midkine overproducers that may regain their sensitivity to THC as the glioma cells did after pharmacological ALK inhibition.
Thank you for your assistance.
I would ask you about maintanance dose of the memantine. Was it actually only 1 mg or this is an error. Bacause simple calculations suggests a 10 higher dose.
I am using EMS for mutagenesis of Neolamarckia cadamba for my fyp. My lab does not have DMSO. So I need other alternative of DMSO
How can I design a study to test the neuroprotective effect of a fruit using albino wistar rats?? Pls can you treat this as urgent??
Thank you for adding your ans
We found that this drug is able to improve memory loss and anxiety and also is able to restore the expression levels of neuroplasticity genes in mice.
i want to test neuroprotection of drug in rat but the dose present of this drug in mice only so what should i do?
I am working with amyloid beta peptide 1-25 to study neuroprotective effect, and before each test the peptide must be aggregated for use, I would like to know how long I can store the aggregated peptide for use in the neuroprotection assay.
To evaluate the neuroprotective effect of a molecule against the beta peptide 25-35, in the methodology the molecule should be applied 2h before the peptide, but the molecule must be extracted from the cell culture before adding the peptide?
Parkin protein importaint bıomarker in neurodegenerative disease and this protein has neuroprotectıve effect in neurodegenerative disease and cancer.
Are training opportunities the main solution for the development of the field of neuroscience in poorer countries?
I have a question regrading permanent MCAO. I am using rats for my experimental model by means of 4-0 nylon with rounded tip (heated manually) and I coat the nylon with poly lysine before experiment. Usually I collect a sample after 24 hrs.
Most of the rats die within 24 hours of MCAO, although there is less bleeding (I take necessary steps to minimize the bleeding) and everything goes normally. The rats awaken after the surgery but are not in a good condition and within 10-14 hours they die.
When I inspect the brain, I notice a very big infarction. Now I am worried that this is why the animals are dying.
At what condition do I have to treat cells with LPS? In serum free media? For how many hours?
Good day. I am about to conduct a neuroprotective studies of an endemic plant extracts using Drosophila melanogaster as animal model. Most of the journal articles that I have read did not use positive control but I just want to know if there are any. Thank you very much.
I saw several journal articles who utilized paraquat and acrylamide for neurotoxicity studies in Drosophila melanogaster. There are more studies which used paraquat but it is more toxic and more difficult to handle dispose compared to acrylamide. What are your thoughts?
I want to do studies on neurotoxicology or neuroprotective properties of natural products. Can you suggest doable bioassay for this? Im thinking of using Drosophila melanogaster. Any thoughts? Thank you for your help.
I am hoping to investigate how administration of a neurotoxic substance affects the blood-brain-barrier in the rat brain, and how a potentially neuroprotective substance attenuates this.
Could anyone please suggest an appropriate methodology for this, or point me in the direction of suitable references?
IHC/IF strategies would be highly convenient!
Thank you :)
I injected a drug (subcutaneous in mice) and I noticed that there was an increase in number of microgias in the hippocampus (IBA positive cells). These microglias are more branched and non-reactive to MHC-II.
How should I interpret this increased in the number of branches and increased in the number of not activated microglia caused by a drug compared to control animals (which did not suffer intervention)? It can be interpreted as neuroprotection phenotype even if they have not suffered any inflammatory stimulus? Is it possible that microglia become more "resting" than those of the control animals that do not have inflammatory stimulus?
Sphingosine-1-phosphate1 (S1P1) regulates various molecular and cellular events in different body parts. Its expression pattern and functions are also varied dependent upon the cells types where it is expressed. Does anyone have any information regarding the effect of S1P1 in brain vasculature? Specially in ischemic condition (many paper suggests activation of S1P1 is neuroprotective in ischemic condition, however they lack the discussion on effect of S1P1 in brain vasculature). So if you have any information regarding the S1P1 signaling in brain vasculature, please do share !!!
Could you please provide me some article which showed improvement of neurological deficit without change in infarct volume or vice versa after drug treatment flowing stroke induction in rodents.
Just recently, features of psychiatric disorders such as schizophrenia were suggested to be due to a decrease of brain memory center’s inhibitory neurons. HSV-infection is primarily limited to mucosal epithelial cells and neurons, and autophagy is critical in antiviral defense in neurons. Given that type I IFN treatment failed to completely block HSV-1 replication and induce cell death in neurons, some xenobiotical factors might be considered triggering replication of neurotropic HSV-1, and lead to a loss of inhibitory neurons.
I'm looking for a suitable human neuronal cell line for neurotoxicity or neuroprotection screening. Which human neuronal cell model is best for high throughput screening? Can anyone help?
Our investigations deal with the searching of antihypoxic and neuroprotective mechanisms of BDNF (Brain-derived neurotrophic factor). Previously we used an antagonist of tropomyosin-related kinase B receptor (a high affinity receptor to BDNF) - k252a, but now we would like to find more specific blocker.
Our lab recently thought of an interesting potential link between a protein of interest and neuronal excitotoxicity. We thought it might be a good idea to do a pilot study in which which we induce seizures in wildtype mice vs transgenic mice and evaluate the seizure-associated apoptosis. However, we have never conducted seizure studies before and our transgenic mice are on a C57Bl6 background. I've read several reports indicating that C57Bl6 mice are resistant to seizure-associated neuronal apoptosis. I found a few articles reporting seizure-induced neuronal apoptosis in C57Bl6 mice, but those are only a few articles and the majority of publications suggest that C57Bl6 mice are resistant. For anyone with experience inducing seizures in C57Bl6 mice, will they truly have little to no neuronal apoptosis even with severe seizures? Or is there a particular drug (kainate vs pilocarpine vs others?), administration method (IP, SC, ICV, etc), and concentration that you would recommend which could stimulate enough excitoxicity to evaluate for neuroprotective effects of the transgene?
Can we adapt the strategies in brain injured patients?
In a recent pilot study, Werndle et al. presented preliminary data of a new technique for the continuous monitoring of spinal cord pressure and the corresponding spinal cord perfusion pressure (Crit Care Med 2014;42:646–655). Their analyses revealed that the use of inotropic drugs for an increase of spinal cord perfusion pressure optimizes neuronal function measured by motoric evoked potentials and muscle strengths below the spinal level of injury.
Are we ready for a routinely monitored management of spinal cord perfusion?
Which mean arterial blood pressure should be targeted in this context?
How long and how invasive should we monitor?
I have multiple breakages on my bands. I use 4% stacking gel, 10-12% separating gel, I block overnight at 4 degrees with 5% nonfat milk in TBST, 1st antibody 1:1000 overnight (santa-cruz), 2nd antibody 1:10000 for 1:30 hr at RT (santa-cruz).
Literature varies about this so I have done some pre-tests. I've done 42C for 2 hours in an incubator but Trypan Blue still show very high viability (>90%) but the cells look very much dead on microscopy. Should I be using a more sensitive assay? or the heat stres condition is inadequate?
I'm searching for a neuroprotective endogenous product, which will ameliorate the toxic insults by LPS.
I am having some difficulties on finding papers related to the effect of phospholipids, such as phosphatidylserine and phosphatidylethanolamine, on brain primary cultures, in terms of neuroprotection, citotoxicity and cell morphology.
It has been seen that brain injured patients with HGH deficiency often suffer with depressive symptomology. My interest is in whether anyone has done a study on this, as this is part of a working hypothesis of mine, that HGH may play a role (through the proliferation and differentiation of stem cells) in maintaining and repairing cognitive functioning,(specifically in the areas of attention, memory) and emotions.
Another hypothesis which is linked to this, is that BDNF and HGH work together in different ways with regards to neurogenesis and neuroprotection, but that both are required to restore functioning. Has anyone done any studies on both of these factors together (there are a great deal of studies on BDNF, but none that I can find that look at both together)?
In the case of both hypotheses, I have not been able to find studies specific to what I have mentioned.
Any comments or input would be appreciated.
Im trying to conduct a neuroprotective assay with SH-SY5Y cells differentiated with RA and TPA to dopaminergic neurons.
There seem to be multiple cell lines capable of similar feats, and some that seem to be used more without differentiation.
Is there any reason to go through the trouble of dual differentiation? or would it be easier and more reliable/reproducible to work with N2A/CATHa/PC12 cell lines, as they seem to be the standard in neuroprotective research.
I understand that SH-SY5Y cells are of human origin, but even still, they dont seem to be heavily used when compared to mouse line.
Luciferase activity assay showed highly significant binding of my drug to androgen receptor, I am planning to do IHC and see whether androgen receptor is over expression in OVX female brain after drug treatment elucidated AR dependent neuroprotective pathway in female in absence of estrogen.
I'm trying out a new neuroprotective substance on animal models of ischemic stroke, so far I could prove that this particular thing could cause caspase 3 activity to decrease at 24h of reperfusion. But my boss wants to see if it also affects other forms of cell death/damage during this time period. From the papers that I've seen so far, 24h to 72h is a pretty nice time span to see apoptosis, too early for autophage and too late for excitotoxicity. Does anyone have any suggestions on where I should look or what papers I should read?
I would like to know in context of Parkinson's disease?
I would like to know whether I should worry about using ethanol as a solvent for testing neuroprotective effects of various agents (especially in parkinson's models), because of its inherent protective effects (lets ignore the vehicle control for now).
As T3 has a positive influence on axonal growth, dendrite branching and development of myelin sheath I wonder if it could be used to increase the regeneration processes in post stroke patients.
Currently I am working on a systematic review with meta-analysis. I will be writing review about the neuroprotective efficacy on a drug. From the extracted papers I collected infarct volume and neurobehavioral score. But now I am facing a problem, some of the results are in mean +/- SD format (7.24 ± 1.04 versus 12.59 ± 1.44mm3) and some are in percentage improvement (47.07 +/- 7.63% versus 26.27 +/- 5.63%). Is there any way I can combine these data to find out effect size and plot a graph? If yes, could you suggest a method or software?
I am studying gender differences following cerebral ischemia, and i have surprisingly noted that NSPCs donot express BDNF after 7 days of ischemia. I performed IHC and co localization studies with Brdu . Has anybody seen the same expression pattern of BDNF?
1) As we all known, in clinical trials,the NMDAR antagonists show prominent neuroprotective effect. However, all of them failed in clinical trials.
2) Why should t-PA should be used within 4.5h?
3) Cortical neurons can be more resistant to hypoxic injury than microglia in a relatively short period according to our own observation.
I am thinking that should a neuron-glia protective strategy should be more reasonable in stroke since that more and more functions exerted by glial cells have been found.
Many literature says that antioxidant system does not play role in neuroprotection in female brain after an ischemic stroke, ROS is generated after stroke in both male and female brain, then how is the neuroprotection observed in female post menopause, has anybody studied any antioxidant enzyme in female brain? Also is there anybody using non-hormone based molecule in female following stroke?
I have no experience whatsoever transfecting cells with cDNA, and I am looking for help/guidance/knowledge from the community.
What electroporation unit do you recommend? I will be using mainly PC12 cells.
Are there particular settings or solutions you like?
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We have used the model of four soft knots on the sciatic nerve and the model of four soft knots on the saphenous nerve, but were unable to generate the expected hyperalgesia. Animals exhibited no significant changes and sometimes presented hypoesthesia.
Does neuroinflammation and neurodegeneration induced by continuous infusion (intracerebroventricular) of LPS occur in all CNS neurons or only in specific regions? The literature is rich in research about the hippocampus, but not on other regions. I have special interest in the hypothalamus.
I have been trying to test the toxicity of Amyloid beta oligomers on neurons by measuring ROS. I am observing that the ROS response on exposure to these oligomers is highly variable when tested even in consecutive experiments as well as with the same oligomer preparation. I tried to characterise the oligomer preparations on Tricine gels which I found to be consistent every time. I want to ask what factors can be there behind this variable response and how to reduce them. Is it also observed by other researchers working in this field?
Neuroprotection is a contemporary approach used in the treatment of glaucoma, retinitis pigmentosa, diabetic retinopathy.
I am asking this with respect to resuscitation from cardiac arrest. Usually autoregulation to CO2 is impaired in this situation. Therefore, if hypercarbia is neuroprotective, what is/are the mechanism(s)?
I also have a problem with detecting the LC3II band on my western blot. The lC3I is not well separated from my LC3II band or the LC3II band is a smear.
I use 4-20%Tris/Glycine gels from Biorad. For the lysis step we use MPER extraction buffer with proteinase and phosphatase inhibitors. I use 75 Volt for the SDS-running, 35 Volt for the transfer time. I also use PVDF membranes. But I do not know if I should change the running, transfer buffer or the lysis buffer for the sample preparation?
Hi every body. If someone is working on the 2 Dimensional gel electrophoresis (2D) USING tissue sample, i have some question regarding focusing step. the focusing result of pH 4-7 give clear spots while with pH 6-9, spots are mostly blurred not clear. Also the region of pH6-7(in pH 4-7 IPG strip) showing no spots while their are in abundance of spots in the reaming gel. similarly the region pH rangining 9/8-9 in ( in pH 6-9 IPG strip) is also blank with no spots while the reamining gel is full of spots..Your worthy suggestions will be greatly appreciated.
I came to know that certain hippocampal cell lines don't express estrogen receptors (such as HT22). I was thinking of working on rodent cell line SCR022, but no information about the presence of estrogen receptors in it. I would really appreciate if you could help me on it. Thanks.
The pathophysiological basis of primary open-angle glaucoma and the factors contributing to its progression are not fully understood. The elevation of intraocular pressure (IOP) is the most important risk factor, and IOP reduction is currently the only evidence-based treatment.
However, some patients develop glaucomatous neuropathy without ocular hypertension. Moreover, some patients keep progressing even with low levels of IOP. Thus, other factors may be involved in the development and progression of glaucoma.
Do you recommend/prescribe anything besides lowering IOP for your glaucoma patients (Ex: nutrition, curcumin, ginkgo biloba, sports, etc.)?
Animals injected IP with my specific chemical end up being protected from perinatal cerebral hypoxia-ischaemia. We have clues about the molecular mechanism, but I would like to know whether the drug itself gets into the brain at all or whether it is a metabolite or secondary effect that is protecting? Is my only option trying radiochemistry?
Many models out there but which is the best for neuroprotection studies? I have some compounds validated using in vitro assays and I am looking for collaborators to test them in other models.
If blood glucose levels are further or strictly controlled up to lower level of normal blood sugar range, Can evoked potential changes be restored?
Do you have any articles regarding the protective effect of Terminalia chebula on the glutamate induced toxicity to the neurons? Both in vitro and in vivo paper will be appreciated. Either the extract or the active principle from the T. chebula.