Science topic

Neuroinflammation - Science topic

Explore the latest questions and answers in Neuroinflammation, and find Neuroinflammation experts.
Questions related to Neuroinflammation
  • asked a question related to Neuroinflammation
Question
1 answer
The method I am looking for should be non-invasive and within the scope of MRI modalities.
Relevant answer
Answer
Why not start with serial observations on how the different forms of neuroinflammation develop, Sneha Majumder?
In possibly considering the famous pieces of evidence presented at www.ms-info.net on the best-studied kind of neuroinflammation?
  • asked a question related to Neuroinflammation
Question
2 answers
Is lipocalin-2 a good guy during neuroinflammation?
There are contrasting reports regarding this protein. Some say it protects the integrity of the BBB during inflammatory conditions other researchers say otherwise.
What do you think?
Let's share some ideas
Relevant answer
Answer
Thank you for the answer. It was helpful. Actually, the paper talked about the bad side of lipocalin-2
  • asked a question related to Neuroinflammation
Question
9 answers
I know this method published in PLoS ONE but do not whether I will be able to use it as I do not have matlab. I will try to use ImageJ or FIJI...
Kozlowski C, Weimer RM (2012) An Automated Method to Quantify Microglia Morphology and Application to Monitor Activation State Longitudinally In Vivo. PLoS ONE 7(2): e31814. doi:10.1371/journal.pone.0031814
Thanks in advance for your help.
Relevant answer
Answer
Try this one.
It's easy to apply, the only thing you need is FIJI.
Regards
  • asked a question related to Neuroinflammation
Question
3 answers
Whether lPS-induced inflammatory can induce mature il-1β secrete?
Relevant answer
Answer
Good question
  • asked a question related to Neuroinflammation
Question
17 answers
I recently had a video created from one of my manuscripts in Neuroglia MDPI entitled:
Hypothesis: Neuroglia Activation Due to Increased Peripheral and CNS Proinflammatory Cytokines/Chemokines with Neuroinflammation May Result in Long COVID. Neuroglia 2021, 2(1), 7-35; https://doi.org/10.3390/neuroglia2010004
Here is the video link:
This video runs about 10 minutes and pretty much tells the story of the manuscript in a video highlighted fashion.
In today's fast-moving internet society and the younger population wanting things condensed for them and increasing use of smartphones all around us the utilization of videos regarding scientific manuscripts might become popular. While the manuscript remains available online and most are available for open free access it might be possible that videos might increase the readership of the full manuscript and that the videos will be sort of like an introduction to invite more readers for viewing the author's work? This is open now for discussion.
Melvin R Hayden
Relevant answer
This will be very exciting and make content more visible and available to a wider audience.
  • asked a question related to Neuroinflammation
Question
6 answers
Hi everyone,
Do you have any experience in preparing sample dilutions to measure the concentrations of inflammatory cytokines (TNFα, TGFβ, MCP-1, IL-1α, IL-1β, IL-6, and so forth) for an ELISA when it comes to any rat brain tissue, especially hippocampus. I'd prefer not to perform a pretest, and waste any well-strips beforehand. Based on your experience from different labs, what would be the expected protein concentration ranges of these cytokines in a supernatant saved from tissue homogenate prepared from a healthy rat (Sprague Dawley) brain tissue (hippocampus)?
Kind regards,
  • asked a question related to Neuroinflammation
Question
3 answers
Hello Experts,
Excuse me,
I would like to ask if we can apply the term "Immunoreactivity" within the spinal cord or within the brain as the alternative keyword to study about Neuroinflammation? And how is the correlation between them?
And is every immunoreactivity tissue sampling method can be included as Neuroinflammation process too?
Thank You in Advanced.
Relevant answer
Answer
So these words aren't replaceable for one another, yes in case of neuroinflammation their is immunoreactivity but immunoreactivity exclusively not the way of neuroinflammation.
  • asked a question related to Neuroinflammation
Question
1 answer
A peer-reviewed journal, Neuroimmunology and Neuroinflammation opened a special issue to publish review articles about recent advances on Parkinson's disease. Please refer the link above to have more information how to submit it. Thanks.
Backil
Relevant answer
Answer
Thank you very much
  • asked a question related to Neuroinflammation
Question
3 answers
I am currently studying a proteolytically stable peptide that transiently increases blood brain barrier permeability. While the results suggest that it could facilitate drug delivery to the brain, we are interested in assessing the potential downside of such a strategy.
Primarily, we are worried about neuroinflammation. My lab does not have the facilities to properly detect neuroinflammation. Does anyone know of any lab, core facility, or private company that offers services that can determine whether or not the peptide we are testing can lead to neuroinflammation?
Relevant answer
Answer
Interesting detail, Gert Fricker - but how to recognize these biomarkers' pathogenic/clinical relevance?
  • asked a question related to Neuroinflammation
Question
6 answers
Hello experts,
I want to ask about CNS in the Neuroinflammation/Neuroimmunology concept.
Is it correct to say that CNS is defined as immune privilege organ due to its unique of immune reaction compare with the general immune system? Is the unique refers to the ability of CNS to induce its own immune reaction, independent from other peripheral immunity, or any other reasons?
And is it still updated to classify CNS as immune privileged system?
Thanks in advance for your answers and comments
Relevant answer
Answer
Fakhruddin Masse Originally thought to be immunologically privileged, now it is accepted that immune cells are present in the meninges and provide immune surveillance of the CNS. However, the unique properties of these lymphatic systems, including their location and size, may explain why immune responses to CNS antigens are often slower than in peripheral tissues.
Reference: doi: 10.1016/j.it.2015.08.006
  • asked a question related to Neuroinflammation
Question
3 answers
I am using an organotypic hippocampal slice culture where we are exposing our slices to alcohol with subsequent alcohol withdrawal.
I want to make sure I am capturing the right time to assess TNFa concentrations. We are currently collecting and assessing 24 hours after the treatment, but I'm concerned that TNFa concentrations may be more transient (i.e. TNFa may act quickly and be subsequently degraded in a window of time that I'm missing at 24 hours compared to something like 30 minutes or an hour after treatment).
Does anyone have any suggestions/can anyone direct me to a reference regarding the optimal window of time for assessing TNFa concentrations?
ELISA details: analytical sensitivity of <4 pg/mL and an assay range of 11.7-750 pg/mL
Relevant answer
Answer
Dear Caleb Bailey
This depends on some variables, e.g., the kit you are using (Invitrogen, Merck, anyway), besides the cell culture you are going to analyze, and the solvent used in the treatment. If the kit manual does not indicate, the ideal is initially to perform a dose-response curve (6h, 12, 24 h ...). I treated overnight with EtOH extract in human neuroblastoma cells (SH-SY5Y) and there was a response. I hope you helped even after a certain time of you question.
Regards,
  • asked a question related to Neuroinflammation
Question
19 answers
Hi
my lab is in São Paulo, Brazil. There is a postdoc position open for the periodo of 12 month, starting in 2020. The plan is to study neuroinflammation caused by SARS-CoV-2 infection in bioprinted neural tissue.
Besides the damages to the respiratory system, studies indicate that the central nervous system is also affected in severe cases of COVID-19. The main symptoms are headaches, seizures, and consciousness disturbance, and necropsies revealed that infected patients show neural degeneration. Infection can result in severe neurological complications such as viral encephalitis, toxic encephalitis, and acute cerebrovascular diseases. The working plan proposes the production of SARS-CoV-2 in a bioprinted neural tissue, followed by the analysis of neuroinflammatory response.
Experience required in 3D bioprinting or brain organoids or 3D culture or culture and differentiation of h-iPSC in neural cells. Knowledge of molecular biology techniques (qPCR, RNAseq), and cellular analysis (immunocytochemistry, flow cytometry, live-cell microscopy) is desirable.
To apply, email me your CV, a letter of motivation and two reference letters. Pre-selected candidates will be invited to a conference call.
Thank you!
mari
Relevant answer
Answer
Three D - Modelling of SARS-COV-2 - https://www.kolabtree.com/find-an-expert/subject/3d-printing . But whether this kind of 3-D Molecular mapping of SARS-COV-2 will lead to some advantages for Vaccine developement ?
  • asked a question related to Neuroinflammation
Question
1 answer
I am trying to isolate lymphocytes and/or myeloid cells for FACS analysis from the cohlea of mice p.n. day 4-16. Considering that there is a lot of hematopoietic bone marrow in the temporal bone itself, even though I microdissect the tissue, I get a lot of hematopoietic cells which, naturally, interferes with my data. Does anyone have any experience with this?
Relevant answer
Answer
Dear Marko,
I have to admit that I'm not experienced with cochlea tissue. What exactly is the problem that prevents you from isolating single lymphocytes or myeloid cells? Are these cell types difficult to distinguish under the microscope? Can you do IHC or immunofluorescence staining to visualize and detect the cells of interest? Or is your microdissection system not precise enough to cut single cells? Which one are you using? Is the laser calibrated well?
Kind regards,
Heidi
  • asked a question related to Neuroinflammation
Question
7 answers
I've been trying various iba1 antibodies with either Alexa 488 or 647 and am getting a lot of background and have never once seen anything close to resembling a microglia. I've tried blocking with various combinations of 0, .3 or 3.0% milk, 0, .3 or 1.0% BSA, with 4% normal donkey serum and nothing has worked.
Any suggestions would be very much appreciated. Perhaps there are better membrane-bound proteins I could stain for?
Relevant answer
Answer
try vector trueview, autofluorescence quenching kit with DAPI (Cat# SP-8500)
  • asked a question related to Neuroinflammation
Question
7 answers
According to researches, appendix might has connection with Parkinson's Disease but consequences are conflict. One study says, appendix removal reduces risk of PD but another study says that it increases.
Uncovering a Link Between the Appendix and Parkinson Disease Risk
doi:10.1001/jama.2019.9041
Thank you!
Relevant answer
Answer
  • asked a question related to Neuroinflammation
Question
2 answers
I've been on neuronal cell culture to study neuroinflammation, but there has been a debate on neuronal cells not being relevance or giving significant role in neuroinflammation. It should have been immune cells like microglial cells.
But what if I want to proceed with neuronal cells, what are the markers that can be used other than inflammatory cytokine and chemokine?
Relevant answer
Answer
Expression of TLR4 in neurons is mostly in non-detectable range (see ). So if you are treating pure neuronal cultures with LPS, you would not see a significant alteration in cyto/chemokine profile. However, in many cases, primary neuronal cultures are contaminated with astrocytes, which does respond to LPS stimulation. A better model would be to co-culture neurons with mixed glia.
  • asked a question related to Neuroinflammation
Question
9 answers
PTSD is associated with inflammation but the cause is unclear. What do you think?. Does neuroinflammation cause the symptoms of PTSD or does PTSD cause neuroinflammation and systemic inflammation?
Relevant answer
Answer
An excellent question, Silvia, thank you.
I have benefitted from the entire thread.
Your original question was, "Is PTSD caused by neuroinflammation or does PTSD cause neuroinflammation?" There is growing evidence that supports the view that inflammation is both a process and a signal. This signal is readily communicated between the periphery and the CNS, as with gut inflammation. When inflammation is induced within the CNS, in humans one commonly finds neurobehavioral changes.
An additional field of consideration that supports this occurrence is that of traumatic brain injury (TBI). Since TBI is still associated with an emotionally traumatic experience, the delineation between the physical and emotional factors is more of a gray matter than black and white. If someone is aware of an experimental model or clinical context in which neuroinflammation is clearly induced without associated emotional trauma, then your cause-and-effect question may find a resolute answer.
  • asked a question related to Neuroinflammation
Question
2 answers
how long does the cerebral cognitive impairment following LPS administration last? if a doses of 250ug/kg/day of LPS is used 055:B5
Relevant answer
dear...maybe the article can help you
Hope this Helps!
  • asked a question related to Neuroinflammation
Question
5 answers
I want to know that whether there is any agent which can suppress the neuroinflammation in brain or not?
In brain, neuroinflammation occurs mainly because of the microglia or astrocytes. So, minocycline can reduce the microglia mediated inflammtion but I want to know something which can reduce the inflammtion cause by both cells i.e. astrocyte and microglia
Relevant answer
Answer
Are you sure you want to block inflammation in the brain by an anti-inflammatory compound? The new paradigm in inflammation research is inflammation resolution which is an active process to resolve inflammation (instead of just blocking it). Inflammation resolution mediators are resolvins, maresins, protectins etc.
  • asked a question related to Neuroinflammation
Question
6 answers
I want to study the demyelination degree of EAE mice. I know that in the EAE model, lesions are preferentially located in the spinal cord and due to that it is very common to use LFB staining for spinal cord. Nevertheless I´m also interested in analyzing the brain. Has anyone used this staining in brain frozen tissue?
Thank you very much in advice
Relevant answer
Answer
Hi Inaki,
LFB may be to colorful to visualize the fiber or demyelination. Better to use silver staining if there is more demylination as it may be less sensitive if there is suttle demylination.
Following article might help you
thanks
  • asked a question related to Neuroinflammation
Question
1 answer
I am working on a combined model of chronic immune activation via LPS and chronic mild stress. There is a discripancy in behavioral and cognitive changes between CMS vs.LPS/CMS and I wonder how LPS exposure could modulate response to CMS
Relevant answer
Check this out:
Int Immunopharmacol. 2002 Mar;2(4):487-97.
Effects of chronic mild stress on lymphocyte proliferative response. Participation of serum thyroid hormones and corticosterone.
Silberman DM, Wald M, Genaro AM.
Abstract
"Stress produces changes in various immune processes. Some of these changes may be due to neurochemical and hormonal alterations including thyroid hormones levels. This work was carried out to study the impact of chronic mild stress (CMS) exposure on proliferative responses and its correlation with serum thyroid hormone levels. In addition, the influence of serum corticosterone levels on these responses was also studied. For this purpose, mice were submitted from1 to 6 weeks to a CMS model. After undergoing the stress schedule for 4 weeks, an alteration in the proliferative response was observed. Lymphocytes from exposed animals showed a decrease in T-cell response to concanavalin-A (Con A) and phytohemagglutinin (PHA) and an increase in B-cell proliferation to lipopolysaccharides (LPS). In parallel, a reduction in T3 and T4 serum levels was observed. On the contrary, serum corticosterone levels increased in animals exposed to CMS for 1 or 2 weeks and then return to normal values. Lowering serum thyroid hormone levels by propylthiouracil (PTU) treatment negatively modulates T-cell response without affecting B-cell response. On the other hand, the substitutive T4 treatment in stressed animals improved significantly the proliferative T-cell response. Non-significative changes in CD4/CD8 ratio were observed neither in stressed, PTU- or T4-treated animals. Taken together, our results suggest an impact of chronic stress on thyroid function that in turn alters T-cell response. "
  • asked a question related to Neuroinflammation
Question
8 answers
Can peripheral blood be used to check neuroinflammation or microglial activation? or Do we have any markers in the peripheral blood which can detected either by ELISA or flow cytometry and give us insight into neuroinflammation or microglial activation? This is for clinical samples.
Relevant answer
Answer
Please consider Glial fibrillary acidic protein (GFAP). It is not definitely neuroinflammation specific but is related to glial cells. We previously found good data in stroke patients.
  • asked a question related to Neuroinflammation
Question
4 answers
Dear all,
I am looking for a procedure to damage the bacterial wall and therefore promote the release of lipopolysaccharides in the culture medium, without killing the bacteria. I need to do this for develop a positive control of neuroinflammation by gut microbiota. Could you please suggest me also a E. coli strain or other kind of bacteria useful for this goal?
Many thanks!
Relevant answer
Answer
  • asked a question related to Neuroinflammation
Question
13 answers
I have been recently trying to isolate primary microglia from mice pups brain (P0-P1). To prepare mixed microglia culture, I used 3 brains for a 75 cm2 flask. After around 10-12 days, astrocyte confluent layer is formed, and many microglia appears. I isolated those microglia by a shaking method (100-120 rpm/ 2 hrs).
At first harvest, I usually get 3-5 x 105 cells per flask. But, after the first harvest, I do not see the growth of new microglia. I only see the microglia that did not detach during the first harvest. Nevertheless, I tried to isolate for second harvest (after 1-2 weeks from 1st harvest), but end up with very low yield (2 x 104 cells).
Is there any ways to increase the yield?
Medium used: DMEM (10% FBS, 1% penicillin/streptomycin)
Relevant answer
Answer
I agree with Clarissa's suggestion. M-CSF (10ng/ml) is very important for microglia proliferation. We did not find the many difference between the 1st and other harvest by using the marker labeling and patch clamp.
  • asked a question related to Neuroinflammation
Question
3 answers
I am using SHSY5Y cells to develop neuroinflammation. I wanted to use MAP2 as a marker, but MAP2 only indicates the cells are differentiated. Is it necessary to ensure the cells are mature (eg: have synapse (synaptophysin as marker) to validate my in vitro model of neuroinflammation?
Relevant answer
Answer
Hi Noor,
Although it is not totally necessary, I would recommend it or I would try both. Non-mature neuronal cells can behave very different and present diverse antigens. However, some differentiation protocols can be a little... "tricky". You can obtain some aberratic cells that can interfere with your results.
Overall, I would do some testing using both to characterize your in vitro model.
Regards,
Jordi.
  • asked a question related to Neuroinflammation
Question
1 answer
Antibody-testing in Susac syndrome - antigen target and availability of analyses.
Relevant answer
Answer
Susac syndrome is one of the differentials we MS specialists keep in mind when we diagnose multiple sclerosis. to date i am not aware of any serologic or CSF test for this disease. it is based on history, physical and MRI which shows the distribution of white matter lesions that is very similar to multiple sclerosis except for some slight differences which can be missed by the untrained eye. thanks.
  • asked a question related to Neuroinflammation
Question
2 answers
Hello everybody,
i am trying to characterise my LPS model (rat) with qPCR analysis to check the level of neuroinflammation, but i have a pretty big variance between the LPS treated animals.
excluding the differences between animals and how the may naturally deal with inflammation, do you think that specifically LPS may act so differently into animals and induce so different responses?
cheers!
Relevant answer
Answer
You should clarify first if it is direct injection into the brain, peripheral ip injection, the dose, serotype and company. Then if you dissect brain regions, if you remove blood before tissue processing and how long you collect after LPS injection.
  • asked a question related to Neuroinflammation
Question
5 answers
I need to find specific pathway for control neuroinflammation .
Relevant answer
Answer
i agree with Nemanja Zdravkovic
  • asked a question related to Neuroinflammation
Question
2 answers
I rearching effect of estrojen on neuroinflammation with TNF-a. I will use JAK-STAT singnaling pathway and I will control differantiated RA Tnf(-), tnf(+) and tnf(+)östrojen(+). I will look at Nf- kappa B gene expression but I need to explain it detalied. How can I find detailed?
  • asked a question related to Neuroinflammation
Question
4 answers
Currently, I am studying about neuroinflammation using murine derived microglial cell line. We focuse to reduce the inflammatory cytokines and inflammatory mediators production. In the near future we also hope to learn about amyloid-β downregulation. Is there any one who could give a suggestion regarding the mechanism linking between neuroinflammation and amyloid-β production ?
Regards,
Relevant answer
Answer
Anyone who has found the linkage would have received the Nobel Prize in Medicine by now! Good luck in your search.
  • asked a question related to Neuroinflammation
Question
5 answers
I've been looking for a suitable model of chronic neuroinflammation, that not involves a Neurodegenerative disease directly. So, I look for LPS model and TBI, wondering which model is better for evaluate chronic microglial activation.
Relevant answer
Answer
Greetings. TBI is certainly a very good way to study chronic neuroinflammation. However, TBI is a spectrum and you need to choose which part of the spectrum is suitable for your studies. mTBI does have inflammation but the degree of inflammation may be too mild for the sensitivity of your studies. perhaps CTE will suit your studies the best and it has tremendous practical, social especially, impact. thanks.
  • asked a question related to Neuroinflammation
Question
6 answers
Hello, we are analyzing inflammatory markers (such as TNF-alpha, IL1B, IL6 and INF-gamma) in brain samples (hippocampus and prefrontal cortex) after an intra-peritoneal injection of LPS in C57BL/6 mice.
Despite the high increments of these markers described in the literature using this method, we obtain very low increments or no changes. We suspect that maybe the fact that our animals are housed in a SPF facility could be interfering. Has anyone using SPF animals had the same problem? Could you give us some advice? 
Relevant answer
hi Eva,
I followed 6 LPS injections (1 mg/Kg/day), sample collection 24h after the last administration. I didnt check the cytokine markers yet.. but i checked the expression of nfkb, ikk, amyloid beta which was expressed high and also the hippocampal LTP was significant reduced. based on these, it is pretty much sure that TNF alpha and IL-6 will be higher in the brain.
could you tell me which LPS you are using?
I am using LPS from sigma
If you are still struggling with the marker expression, then i recommend you to initially check the blood serum cytokine levels.
have a nice day
  • asked a question related to Neuroinflammation
Question
2 answers
I am performing a study in which adrenalectomized (ADX) animals are going to be introduced to a chronic stress protocol and then having its corticosterone (CORT) levels analyzed a few days after the stress protocol. However, there is a growing field of literature reporting that ADX already induces severe neurodegeneration and neuroinflammation in these animals after 1-2 weeks (which are fewer days than what I intend to do). Thus, adding exogenous CORT would be an important control in such case.
I would like to have advice or previous experiences of researchers that did such work and their methods of controlling for CORT in this case. Thank you very much.
  • asked a question related to Neuroinflammation
Question
2 answers
I am searching for the base of diseases with unkown course. I want to understand the base of low grade inflammation and the molecules involved in it. 
Relevant answer
Answer
 Nlrp3−/− mice exhibit  defect in development of Th1 response(Gris et al. 2010) and NLRP3 seem to trigger a Th2 bias (Gurung et al. 2015; Daley et al. 2017). But my guess is this behaviour is tissue/cell dependent and so the jury is still out.
1.       Daley, D., et al. (2017). "NLRP3 signaling drives macrophage-induced adaptive immune suppression in pancreatic carcinoma." J Exp Med 214(6): 1711-1724.
2.       Gris, D., et al. (2010). "NLRP3 Plays a Critical Role in the Development of Experimental Autoimmune Encephalomyelitis by Mediating Th1 and Th17 Responses." The Journal of Immunology 185(2): 974-981.
3.       Gurung, P., et al. (2015). "An NLRP3 inflammasome-triggered Th2-biased adaptive immune response promotes leishmaniasis." Journal of Clinical Investigation 125(3): 1329-1338.
  • asked a question related to Neuroinflammation
Question
2 answers
I am looking for a way to use fluorescent microscopy in order to measure the levels of hydrogen peroxide in C. Elegans which exhibit Alzheimer’s symptoms like neurodegeneration.  It is ok if there are two separate strains which specifically have some sort of marker for either hydrogen peroxide, catalase, or oxidative stress.  Also, if you mention any strains, please link the article from which it is from.
Thanks in advance
Relevant answer
Answer
Dear Mir Alam,
Oxidative stress can be measured using any C. elegans strain. Our group uses DCF-DA as a fluorescent probe to measure ROS accumulation, not specifically H2O2. I just tried the previous method for N2, CF1038 and GR1307, but I guess it would also work for Alzheimer’s-related-strains, such as CL2006, CL4176, etc.
  • asked a question related to Neuroinflammation
Question
13 answers
Please I need your experience in understanding the role of Autophagy in Alzheimer's disease and if it could be a potential target for finding a cure for AD.
Relevant answer
Answer
Stress to endoplasmic reticulum (ER) can cause UPR and aggresome formation. Aggressome accumulation has been shown in AD. The ER stress is also related to autophagy. So theoretically autophagy can be a target for AD treatment. The thing is when you start to study a new signaling pathway in a disease there is always some association. The issue becomes how to decipher your findings.
  • asked a question related to Neuroinflammation
Question
3 answers
I am an MRI physicist, who is trying to understand the role of glutamate in neuro-inflammation. Since I have a limited understanding of biology/biochemistry, I would appreciate if someone can help me understand the role of glutamate in the inflammation.
I found the following overview very informative: (http://neurotransporter.org/glutamate.html ); however, it still fails to explain my basic question:
i) Does excessive extra-cellular glutamate always means that ONLY inflammation related processes are contributing? Could there be other contributing processes?
I would appreciate if someone can help me understand this. 
Regards,
Dushyant
Relevant answer
Answer
Other processes are related to increased levels of glutamate in extracellular space (ECS).
Under physiological conditions, glutamate is taken up by astrocytes (AS), which convert it into glutamine and deliver it back to neurons as an alternative energy source. However, under pathologic conditions, is excessively produced and AS cannot remove glutamate from the ECS. That produces excitotoxicity. Consequently, free glutamate binds to neuronal receptors, e.g.NMDA, inducing the influx of Ca²+ and Na+ and the efflux of K+ (ionic disturbance). This ion imbalance causes depolarization of the cell membrane and overload of intracellular Ca²+, which leads to mitochondrial dysfunction, decreased ATP synthesis, energy failure, and cell death. Mitochondrial dysfunction is followed by ROS production; wich causes oxidative stress. 
  • asked a question related to Neuroinflammation
Question
2 answers
I plan to study about the mechanism of anti neuro inflammation using cell culture method. My senior has conducted a similar experiment using mouse microglia MG6 cell line, but I want to uderstand the mechanism if the culture is changed by BV2 cell line, is there any signifficant differentiation between those cell culture type ?
Relevant answer
Answer
With all due respect, please use primary cells. BV-2 are, at best, poor replacements for the real thing. Can you gather lots of data quickly with cell lines? Sure. Is any of that data relevant? Not much. Just because a cell produces cytokines with TLR stimulation doesn't make it an actual factual immune cell.
  • asked a question related to Neuroinflammation
Question
6 answers
I used LPS to induce the inflammation response of human vascular smooth muscle cells, but I found that the control group (without LPS treatment) also express obvious COX-2 protein, so it means the cells had already in inflammation state
Relevant answer
Answer
Thank you very much, I will try and to see if it works for my cells, in addition, I plan to use add the TGF-β and IFN-γ to induce the inflammation response, I cultured the HUMAN vascular smooth muscles, so what kind of TGF-β and IFN-γ I need to choose,  I mean HUMAN recombinant or MOUSE recombinant one? Thank you!
  • asked a question related to Neuroinflammation
Question
6 answers
Among the drugs used for MS, few like IFN-beta, Natalizumab, Glatiramer acetate don't cross BBB while Fingolimod do. So a humble request to the experts for their comments.
Relevant answer
Answer
There is a hypothetical target, a subgroup of
B lymphocytes (David Hafler, Kevin O Connor
et al.) which ripen in the lymph nodes of
the cervix. They can be fought outside
the central nervous system.
Regards,
Joachim
  • asked a question related to Neuroinflammation
Question
2 answers
Has anyone used the tubes with gradient centrifugation to help separate out PMBCs ? Was the yeild as good or better than using the longer spin and no brake. Is it really that simple, you poor off the top later? Alll seems too good to be try - but expensive. I have some samples to try but would appreciate some prior knowledge
Thanks! 
Relevant answer
Answer
I used Lymphoprep for PBMC isolation, and the PBMC layer was easily collectable after centrifugation.
  • asked a question related to Neuroinflammation
Question
18 answers
At what condition do I have to treat cells with LPS? In serum free media? For how many hours?
Relevant answer
Answer
Hi Sagar,
Here is the protocol I use for BV2 or primary microglia cultures:
NO assay
Prepare Griess reagent:
2.3ml Phosphoric acid (85%)
1g Sulfanilamide
0.1g Naphtylethylenediamine
97.7ml water
Vortex. Prepare Griess reagent at least half a day before use. Protect from light.
Keep media from cell cultures on ice.
Prepare standards from sodium nitrite (NaNO2): from 0 to 1000 µM. Use the culture media for dilutions.
Pipette media and standards 50µL/well on a 96w-plate.
Add 50µL of Griess reagent on top of each sample. Shake for 10min and protect from light.
Measure absorbance at 540nm in the reader machine.
Good luck,
Sighild
  • asked a question related to Neuroinflammation
Question
11 answers
When he gives extract orally for 14 days and challenged by lps once, and performed novel object recognition. When he analysed his data,  results was not dose dependent 100  and 200 mg is dose dependent but they declined in 400 mg but toxicity studies says (literature) LD may be up to 2000 mg. So what are all the possible reasons for this case.
Please share your suggestions
Thanks in advance
Relevant answer
Answer
what do you mean by "extract" and "challenged by lps" ? I don't understand what you are asking.
  • asked a question related to Neuroinflammation
Question
3 answers
Can anyone help me to find how pathologists calculate neuroinflammation in hematoxilin- eosine sections? how many factor do they measure in order to prove inflammation and apoptosis in rat hippocampus ? I know nothing in these area and I will be appreciate if someone help me to extend my knowledge and there is something else I want to know. Is it acceptable for article referees to calculate neuroinflammation in H&E section by myself?
Thanks
Relevant answer
Answer
Dear  Ahmad
Thank you for your answer. It would be great if you explain me in detail about H&E method of neuroinflammation detection in rat brain. I have to measure inflammation in H&E stain sample of rat brain. I know there is some standards for this goal but I am not neuro-pathologist and I do not know how to study and what book is best in this case
  • asked a question related to Neuroinflammation
Question
7 answers
Does anyone know of a recent paper that lays out the state of research on factors affecting glial transcription, especially as related to neuroinflammation? I would love to have a list of different signals and their effects.
Relevant answer
Answer
Hi Cooper,
Glad the papers have been somewhat helpful in researching glial changes under inflammatory conditions.
It's one of the references within the papers you've already linked, but have you looked at Hickman's 2013 paper (http://www.ncbi.nlm.nih.gov/pubmed/24162652)? Could serve as another resource regarding how microglia specifically change responses at different ages (with the underlying implications of different inflammatory responses).
Good luck in your search! 
  • asked a question related to Neuroinflammation
Question
11 answers
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?
Relevant answer
Answer
There is also an excellent new paper out from Marie Eve Tremblay showing a new type of microglia (called "dark" microglia based on their EM appearance) that becomes abundant during pathological states such as chronic stress, aging, Alzheimer's, etc. They display signs of oxidative stress, but also have highly ramified, thin processes, so it sounds like they may be relevant for your question. See paper below:
Glia. 2016 May;64(5):826-39. doi: 10.1002/glia.22966. Epub 2016 Feb 5.
Dark microglia: A new phenotype predominantly associated with pathological states.
Bisht K1, Sharma KP1, Lecours C1, Gabriela Sánchez M1, El Hajj H1, Milior G2, Olmos-Alonso A3, Gómez-Nicola D3, Luheshi G4, Vallières L1, Branchi I5, Maggi L2, Limatola C2, Butovsky O6, Tremblay MÈ1.
  • asked a question related to Neuroinflammation
Question
9 answers
I've been culturing mixed glia and getting microglia from them for years, but it's always struck me that they look slightly yellow under the microscope. If you take a lysate of microglial cell as well, if you look at it, it is yellow-tinged too! Does anybody know what it is that the microglia are full of that gives them this colour? I've never seen this with any other cell type. Thanks!
Relevant answer
Answer
Hi Marc. That is interesting! I have never noticed the microglia being yellow. I wonder if it is due to their high expression of the NADPH oxidase, which contains FAD that should be yellow. I think this contributes to the yellowness of neutrophils. It might be worth taking a spectrum, and comparing it to FAD and FMN.  These are also fluorescent, so might be worth taking a fluorescensce spectrum.  If it does not fit a flavin spectrum, you could compare it to lipofuscin?
  • asked a question related to Neuroinflammation
Question
6 answers
I am planning to do some experiments in which I need to determine the levels of neuroinflammatory markers such as IL-6, TNF-alpha and IL-1beta in mice brain. 
Relevant answer
Answer
Dear Gaurav,
I'm actually performing RT-PCR, and I think that if you got primers, mixes and homogenate tissues, you are ready to work; In a couple of weeks you can already have some results. Maybe amygdala takes longer, because it is a very little area, with not too much RNA; so it request lyophilization before working.
Anyway I could help you.
Wishes
Maria Rosanna
  • asked a question related to Neuroinflammation
Question
4 answers
As research says neuroinflammation is one of the key factor in epilepsy and HMGB1 is one of the important biomarker. Can HMGB1 rapid diagnostic test in blood can be used to differentiate between epilepsy and seizures???
Relevant answer
Answer
There is a rather quick & yet informative review, downloadable as a lecture in the following link. I hope you find it useful.
  • asked a question related to Neuroinflammation
Question
3 answers
Hello everyone! I would like to find a lab host to participate to TALENTs grant. It is a ìn european grant that provide salary for 18 months, divided in 12 to spent in an Host institution and 6 to return to my base institution. I'm looking for an host laboratory situated in one of following country: Slovenia*, Croatia, Bosnia and Herzegovina, Serbia, Montenegro, Albania, Greece, Germany, France, Austria, Switzerland, Liechtenstein. The laboratory, given my CV, should ideally work in neuroinflammation / neurodegenerative diseases or I would like to learn CRISPR/CAS9 system...details in the link attached..
thanks for all the possible answers! 
Relevant answer
Answer
Dear Fulvio.
Sorry, I asked you, is it other program in EU or the first, you got grant ?After that you are looking for placement?
Thanks
  • asked a question related to Neuroinflammation
Question
5 answers
How can we measure the role of activated astrocytes in neuroinflammation?
Relevant answer
Answer
Hi Lalita,
Since more than ten years, our lab's members work on glial cells (microglia and astrocytes) in neuroinflammatory conditions. On what samples are you working: primary cultures ? in vivo experiments ? brain slices ?...
  • asked a question related to Neuroinflammation
Question
8 answers
Does anyone know any mild model to induce neuroinflammation different from LPS model in rats?
Relevant answer
Answer
Also consider the type of immune reaction you are after (e.g. involvement of specific cells and acute inflammation versus chronic/prolonged). I have found that microglia react very quickly and easily to single cytokines or other toxins, while astrocytes often require a cytokine cocktail (e.g. TNF-alpha + IL-1beta). If you are after a chronic inflammation, then initial microglial activation can also lead to astroctye activation over time. 
  • asked a question related to Neuroinflammation
Question
6 answers
To improve data and reduce variability i would like to move away from outbred strain (Sprague Dawley) and use inbred rats. But it is nearly impossibly to work out which strain to use from the available ones: Lewis, Long Evans, Fischer, Kyoto and many more. I know, for example, that Lewis rats are used for some neuroimmunology (EAE model) but this is different to our model (effect of systemic LPS on the brain) and therefore might not be directly relevant. Do people have any experience with this type of work and inbred rats?
Relevant answer
Answer
Dear Diana,
As mentioned above i recommend the dark agouti rats. They are an invred strain that are great for reliable EAE research as immunisation with IFA and recombinant MOG is sufficient, you dont require further addition of pertussis or other complete adjuvants. 
  • asked a question related to Neuroinflammation
Question
1 answer
We are going to do improvement of cancer chemotherapy drugs-induced cognitive impairment and peripheral neuropathy via inhibition of neuroinflammation and oxidative stress by using natural compound. We will use paclitaxel as a chemo drug. We are searching for doses of paclitaxel in rat which is related to human.Thank you.
Relevant answer
Answer
আমার পক্ষে এক্কেবারেই অসম্ভব ব্যাপার...দুঃখিত ভাই...!!
  • asked a question related to Neuroinflammation
Question
6 answers
Macrophages are known to be an active player in MS. They are involved in active demyelination and myeline uptake, which leads towards the development of foamy macrophages with M2-like properties. But can they migrate out of the brain/lesion before they become necrotic and cause a pro-inflammatory respons (cfr. atherosclerosis)?
Relevant answer
Answer
Foamy macrophages (gitter cells) do migrate out of the MS plaque into the perivascular space and then into the blood stream.
  • asked a question related to Neuroinflammation
Question
2 answers
I'd like to demonstrate that some medicine could reduce the neuroinflammation in ICH model via in vitro and in vivo study. Could raw 264.7 macrophages be used in vitro study instead of BV2 microglia (because microglia was infected by mycoplasma)? What are  the differences  between them ?
Relevant answer
Answer
Microglia cells are specialized macrophages that exist only in the brain. Raw 264.7, in contrast, are general mouse macrophages. There are numerous differences between the different types of macrophages. I think if your disease doesn't cause infection of the brain, but rather other tissue macrophages, then the RAW cells would be the better option
  • asked a question related to Neuroinflammation
Question
7 answers
I am considering using a scholl analysis (using imagej software) but I was wondering if anyone has any better ideas.  I only need to determine if the microglia are activated, I don't need to describe their morphology in detail.  
Relevant answer
Answer
If you also have IBA-1 stained control sample then you can compare IBA-1 staining intensity between them. Activated microglia show increased IBA-1 staining. You can also quantify staining intensity in ImageJ. This is one of the simplest ways.
  • asked a question related to Neuroinflammation
Question
7 answers
If you are aware of the fact that cancer patients treated with standard chemotherapy over the past 20 or so years have cognitive problems with reasoning and motor skills, I'd like your input on why, and why ten to twenty years later.  Microglia (brain macrophages, which is a misnomer) can initiate the process of neurodegeneration, which leads to ex-cancer patients, who've survived through chemotherapy, down the path of significant brain damage.  There is an initial insult due to systemic inflammation, but I'm thinking that endothealial damage and their ability to secrete inflammatory lymphokines perpetuate or exhasterbate chemotherapy-induced cognitive problems in cancer patients.
What do you think?
Michael
Relevant answer
Answer
Yes. I agree with Dr. Lewis Alan Opler. 
  • asked a question related to Neuroinflammation
Question
2 answers
Concerning SPIO and macrophages in neuroinflammation.
What is the safe dose and how to assess the toxic effect of SPIO on macrophages   in vitro?
Relevant answer
Answer
I think the general answer is yes, everything a phagocyte will recognize and internalize will affect the cellular activity and in this case presumably its polarity. How it will affect the cells depend on the size of the particles, how many particles are taken up, particle surface composition, and of course external stimulations e.g. from other cells. This being said, many are using these SPIOs with no or little effect on cells, or at least on the measures they have set. Viability and/or apoptosis assays should be used.
What will happen in your case is difficult to predict, and why a control must always be included,with your specific purpose in mind.
  • asked a question related to Neuroinflammation
Question
4 answers
I am researching into in vitro models linked to inflammation and depression, not ex-vivo or from primary microglia.
Any help would be appreciated.
Relevant answer
Answer
Dear Katrina,
Hopefully some references cited in the article of Najjar et al. might be helpful for you.
Najjar S et al. Neurovascular unit dysfunction with blood-brain barrier hyperpermeability contributes to major depressive disorder: a review of clinical and experimental evidence. Journal of Neuroinflammation 2013;10:142.
Kind regards, Matheus Arts
  • asked a question related to Neuroinflammation
Question
7 answers
I am looking for a protocol to quantify proteins in the mice brain by western blot technique. I want to see the effect of treatment on AD pathology and neuroinflammation markers. I would like to analyze following proteins: Tau, BACE1, COX-2, GFAP, IL-6, IL-1beta, TNF-alpha, iNOS and p38 MAK. Can somebody share with me the wetern blot protocol with all necessary details. Thank you in advance.
Relevant answer
Answer
Dear Gaurav Please find protccol and composition of gel preparation. Protocol is attached.
Good luck
  • asked a question related to Neuroinflammation
Question
5 answers
Does somebody have experience in inducing the microglial activation by systemic LPS injection in rats? Mice seem to respond well to LPS, but rat do not demonstrate neuroinflammatory changes in response to i.p. LPS injection. The data in PubMed concerning this issue are very sparse, but there is still a possibility that some negative results remained unpublished.
Relevant answer
Answer
Hello there
I personally studied this topic. By injecting LPS 2 mg / kg ip to C57BL6 micee, you obtain a clear  neuroinflammation 24-28hrs after injection. Microglia are activated, proinflammatory cytokines increased, in different brain regions.
  • asked a question related to Neuroinflammation
Question
5 answers
.
Relevant answer
Answer
In my experiments I have used CD11b to show immunologically active microglia where as  IBA-1 is constitutively produced in both ramified and amoeboid microglia that may or may not be immunologically active. If you are looking to quantify numbers of microglia I would choose IBA1. However, if you are looking to quantify numbers of activated microglia I would choose CD11b. Just a caution-- I have had issues getting a good IHC with CD11b from Abcam.
  • asked a question related to Neuroinflammation
Question
7 answers
First it was the death of dopaminergic neurons as a result of "oxidative stress". Then the misfolding of α-synuclein. Now there si a suggestion
I had a 2 week course of prednsiolone (30mg.day) last September for an unrelated condition and am now on an 8 week course of budesonide (9 mg/day) these abolish all joint stiffness and pain and I can now climb stairs easily, turn over in bed without having to plan it and gather strength, leap out of chairs and look over my shoulder. I still walk slowly and still fall over more than I used to and my speech is no better but I'm not mildly incontinent any more!!
I was for a week taking 5-amino salicylic acid and this was, I think, just as effective.
It looks as if some PD symptoms are caused by inflammation and may be easily and safely treatable. I found references to inflammation in PD:
but I cannot see any clear connection to α-synuclein.
Is there a coherent story somewhere or are we dealing with more than one related but separate conditions with different causes?
Relevant answer
Answer
I was interested to read that not only is α-synuclein found in colon of PwP but so are Lewy Bodies (http://www.ncbi.nlm.nih.gov/pubmed/23017648).   It also seems that diarrhoea is often associated with PD (http://www.plosone.org/article/info%3Adoi%2F10.1371%2Fjournal.pone.0012728#s1).  In an RG thread on Serotonin and Dopamine William Wilson introduced me to the role of enzyme co-factors, which links serotonin synthesis to dopamine (see file).  (William warned me that one of the authors had been struck off for self medication and that urinary levels of neurotransmitters are not a reliable indicator of CSF levels but this does not invalidate the interconnectedness of the cofactors.)  It is this that offers potentially a way to understand why PD has so many manifestations.  It still leaves us (me, anyway) unsure as to whether misfolded α-synuclein is a cause or a symptom of PD and, if it is a cause, then its role in the process.
  • asked a question related to Neuroinflammation
Question
8 answers
I trying and struggling but not able to stain properly as I used Iba1 and GFAP.
Relevant answer
Answer
Hi Pete,
I am pretty sure that NGF, CNTF, MAP2, VCAM, TNFalpha, TGFbeta, are not specific to astrocytes. If you want Astrocyte specific, stick with GFAP, S100B (which is constiutively expressed in the healthy adult brain), and AldhL1, Glutamine Synthetase, EAAT1 and or EAAT2.
  • asked a question related to Neuroinflammation
Question
9 answers
I am facing problems while counting Iba 1 positive cells in mouse brain section. I cut the brain slices in 20 micron thickness and performed immunohistochemistry. And now I have to perform the quantification of Iba 1 positive cells in the sections. A senior researcher just suggested to count all cells present in the photographs of the both cortex and striatum. But I think this is not the appropriate way of counting. For your convenience, I have attached a photograph here. Could you please let me know how many Iba1 positive cells are present there? Remember the thickness of the slice is 20 micrometer.
Relevant answer
Answer
Hello all
I count all type of cells using stereological techniques. Based on stereology rules, it is best to start with tissues that are 40um. why? becuase tissue get dihydrated 50%, so you end up with 20um thickness of your tissue once it have been stained IHC. then, I use either optical fractionator probe in my software or the cavalieri probe. If you dont have access to a software like that, you can do count of 1 in every 6 sections, for a total of 8 to 10 section per animal. Do a total count in a 5 ROI of 50um by 50um or 100 um by 100 um depends on how big is the hole area you want to count then average the count. the bigger the area the bigger the ROI.
If interested in more details, you are welcome to look at my publications.
i hope this helps.
thanks all
Sandra
  • asked a question related to Neuroinflammation
Question
5 answers
Is it possible that rats and mice differ in their susceptibility to LPS (E.coli) effects? We have mentioned serious microglial activation in the brain (increase in the number and cell area of microglial cells) after intraperitoneal LPS injection in mice (2 mg/kg), but rats (Wistar) seem insensitive to LPS under the same conditions (I mean, in the CNS - no activation of microglia measured by cell area and cell number). It was rather surprising to us since we did not suspect such an inter-species difference in the course of inflammatory response. Do you have any assumptions about why it could happen, given that all experimental conditions were similar for rats and mice? Has anyone noted the difference in the timecourse and/or intensity of inflammatory response between these species? I would be grateful for any ideas.
Relevant answer
Answer
I think that this will basically depend on the pattern of expression of TLR4 in each animal and the cascade initiated after it. So in theory, it can be very different.
  • asked a question related to Neuroinflammation
Question
21 answers
And neurodegeneration in mice.
Relevant answer
Answer
There are multiple ways to assess neuroinflammation. You can perform immunohistochemistry by using specific markers for microglial activation (Iba1) , astrocytic response (GFAP), and neuronal loss (NeuN or Fluorojade for dying neurons). You can also look at the levels of various cytokines that are upregulated during inflammation (TNF-alpha, Interleukins, TGF-beta, and so on).
  • asked a question related to Neuroinflammation
Question
2 answers
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.
Relevant answer
Answer
As you know LPS mediated inflammation is closely associated with nitric oxide production and up regulation of iNOS production at most sites all of which has considerable publications documenting LPS effect on inflammation. Other mediators also play a role. Systemic administration of LPS also produces change in the Nucleus Tractus Solitarii. There is a lot of literature supporting communication pathways between the immune system and brain. I have attached one for your consideration. You are treading on unknown territory as best I know and very interesting work, I look forward to hearing more.
  • asked a question related to Neuroinflammation
Question
2 answers
TNF alpha concentration, its duration, and the activated mechanism can produce opposite effects, both protective or noxious. (Montgomery 2012)
Relevant answer
Answer
Thanks for your kind answer.
According to (Santello 2011 and 2012), very low concentration of TNF-alpha (about 100 to 600 pM) controls glutamergic gliotransmission in the Dentate Gyrus and control synaptic plasticity which is underling for learning and memory. Furthermore lack of TNF-alpha lead to suppress the astrocyte effect and impair LTP.
  • asked a question related to Neuroinflammation
Question
2 answers
Tumor necrosis factor alpha (TNFa) promotes synaptic scaling and gliotransmission at glutamatergic synapses via complementary post and presynaptic actions (Santello 2012).
increasing AMPA receptors lead to more excitation of post synaptic neuron and result of that is exit more K+ from neuron which maybe have effects on astrocyte. But what effects?
Relevant answer
Answer
thank for your kind answer. the problem is that. increasing AMPA receptors lead to more excitation of post synaptic neuron and result of that is exit more K+ from neuron which have effects on astrocyte. I think that may saturate astrocyte.
  • asked a question related to Neuroinflammation
Question
1 answer
A-804598 is an antagonist for P2X7 receptors. We're trying to find out if there's an in vivo data in relation to toxicity for this particular antagonist. Please let me know if there's anything, much appreciated.
- It's an 8 weeks chronic mild stress mice model, interest being the polarization of microglia/macrophages and NLRP3 inflammasome activation in CNS. Administration route is via gavaging syringe. (updated 08/04/2014)
Relevant answer
Answer
Is a radioligand important? If not, you could use Brillian Blue G (IV) as a selective P2X7 blocker and then do immunohisto for analysis. BBG is very similar to blue food coloring so it is rather safe. Sorry I don't know more about your specific compound. All the best in your research.
Jiang L-H, Mackenzie AB, North RA, Surprenant A. Brilliant Blue G Selectively Blocks ATP-Gated Rat P2X7 Receptors. Mol Pharmacol 2000; 58: 82–8.
Peng W, Cotrina ML, Han X, Yu H, Bekar L, Blum L, et al. Systemic administration of an antagonist of the ATP-sensitive receptor P2X7 improves recovery after spinal cord injury. PNAS 2009; 106: 12489–93.
  • asked a question related to Neuroinflammation
Question
4 answers
I am attempting to measure brain inflammation in lysates from cortex tissue. Is there any test that is a good "overall" measure of brain inflammation from these lysates?
Relevant answer
Answer
Look into publications of Jens Zimmer
  • asked a question related to Neuroinflammation
Question
2 answers
Neuroinflammation brain
Relevant answer
Answer
Thanks!
  • asked a question related to Neuroinflammation
Question
7 answers
A mouse model required to study inflammation caused by Alzheimer's disease.
Relevant answer
Answer
Multiple genetic models of Alzheimer have been described using gene knockouts, missense alleles and expressed transgenes:
Many of these are commercially available (including from non-USA repositories) or were developed by academic researchers who may be willing to send you some animals privately or as part of a collaboration. I can help you find a good one if you are interested.
  • asked a question related to Neuroinflammation
Question
4 answers
see above
Relevant answer
Answer
well, neuroinflammation comes in may flavours and it depends on what you really want to study. systemic administration of lipopolysaccaride from bacterial sources causes a strong inflammatory response through the body, including blood-brain barrier leakage and among others, triggers microglia activation and infiltration of immune cells into the brain (see for example: http://www.ncbi.nlm.nih.gov/pubmed/23468966). otherwise, you have to go for specific disease models (EAE for myelin, coriomeningitic virus for encephalitis, anyone for neurodegeneration....). good luck...
  • asked a question related to Neuroinflammation
Question
4 answers
Which important considerations are there post-sepsis in terms of physical weakness if one is interested in a sports intervention?
Relevant answer
Answer
Rehabilitation for everyone and especially to those with sepsis should start as early as possible , starting from ICU and cont;inue after ICU discharge!!
  • asked a question related to Neuroinflammation
Question
5 answers
I still don't know what kind of injection I am going to perform (intraperitoneal or intracerebral) to obtain the best staining.´Does anyone has experience in what could be the best way of injection/timing of LPS? Thanks!
Relevant answer
Answer
Simone, could you let us know what the aim of your experiment is as they will determine the best advice to provide? LPS by either route will certainly elicit a robust Iba; within an hour for ICV and 4 hours for IP.
  • asked a question related to Neuroinflammation
Question
8 answers
Could someone suggest a highly sensitive, cost effective and efficient assay for estimating the secreted cytokines in body fluids or culture media. ELISA can be one alternative, but i have heard there are certain other colorimetric methods which are more Sensitive and accurate. Any leads, please?
Relevant answer