Medical Neurosciences - Science topic

Would anyone be able to sent the drivers and software to my email?

Hello,

The administration of adeno-associated virus (AAV) vectors via intracerebroventricular (ICV) injection necessitates careful consideration of the vehicle used to ensure optimal delivery, stability, and efficacy of the vector. The choice of the vehicle is crucial as it can significantly influence the distribution, expression, and overall success of the gene therapy.

In conclusion, while PBS and aCSF are commonly used and generally effective vehicles for ICV injection of AAV vectors, the final choice should be guided by the specific requirements of the AAV serotype, the experimental design, and the need to maintain the physiological integrity of the brain tissue.

This list of protocols might help us better address the issue.

Maybe the Recombinant Human R-spondin-1 (RSPO1) provided by CUSABIO works for you. The activity has been validated. Here is the link:

Please have look on our(Eminent Biosciences (EMBS)) collaborations.. and let me know if interested to associate with us

Here is our lab page: https://www.eminentbio.com/home/members

Here is our publication: https://www.eminentbio.com/home/Publication

Our recent publications In collaborations with industries and academia in India and world wide.

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Sincerely,

Dr. Anuraj Nayarisseri

Principal Scientist & Director,

Eminent Biosciences.

Mob :+91 97522 95342

Dear Alothman,

First I congratulate you for your motivation of the research. The following important point must be in your mind. There are often times when added research would be required to make it easier for a study to go forward. Your research plans could include an analysis of the methods of study that could work in the future and what points about a topic could be reviewed in such studies. The recommendations that are incorporated into your paper can certainly be important to your work. Be certain when writing your paper that you have clear recommendations that are easy to follow and can be utilized right and are not overly complicated or tough to use in some way.

Regards.

Dear Dr. Ebada,

We know very little about COVID-19 at this moment and its effects on the developing and/or mature brain. In general viral infections can impair charnolophagy (CB autophagy) which is the basic molecular mechanism of intra-cellular detoxification (ICD) for normal function to remain healthy. By attacking the most sensitive neural progenitor cells in the brain, the virus can alter their pluripotency and induce charnolosome (CS) destabilization implicated in inflammasome (particularly NRLP-3) activation to induce hypercytokinemia and charnoptosis (CB apoptosis) implicated in pyroptosis, apoptosis, and necrosis of sensitive hippocampal and other CNS neurons by releasing Panx-1, Viroporine, and gasdermins to cause Charnoly Body Molecular Pathogenesis (CBMP) implicated in early morbidity and mortality through its general (Viral) lytic cycle.

For more details, you may please refer to my books " The Zika Virus Disease: Prevention and Cure" The Charnoly Body: A Novel Biomarker of Mitochondrial Bioenergetics" Fetal Alcohol Spectrum Disorder; and Nicotinism and Emerging Role of E-Cigarettes. I wish I could write more about it.

Dr. Ebada, It is all about Environmental Sanitation, our own Life-Style, Immunity, Mitochondrial Bio-energetics and intracellular detoxification through charnolophagy (CB autophagy), which is compromised by COVID-19 through CS destabilization to cause early morbidity and mortality by infecting the CNS. Thanks.

With Warm regards,

Sushil Sharma, Ph.D; D.M.R.I.T

Academic Dean

American International School of Medicine

Guyana, South America

.

I also need to determine the minimum cluster level with Monte Carlo simulation, but I don't know to use the AFNI program at all. Is there any way I can do this analysis without using AFNI?

when a person is in coma you should not say what you would not say when the person is awake.

I stand by my original statement Ugo Carraro but you have a very lovely outlook on the younger generation. We can always learn from each other.

Great initiative. I will be happy to provide statistical analysis power and research methods...

Thank you, I will follow your advice.

In the meanwhile, I would like to know: in an fMRI the scanner collects a sequence of slices (from different angles, right?) and save them as .dcm files (for example). Thus I have a 2D images each representing a different slice.

In which moment, we have the 3D volume for each particular time instant? Which is the processing step that do this? With the DPARSF toolbox I converted the dicom files for a subject in a NIFTI file. This Nifti file is a 3D matrix 64x64x3526. where 64x64 is the size of each slice and 3526 is the number of slice. Is it normal? Because of course, this is not a volume of voxel (the one I would like to have).

In the early stage, AI considered the emulation of human process. Currently, this paradigm diverges from this

Ting - it is difficult to answer your questions without knowing a bit more about the cognitive / neural processes that you are interested in, but I will try to share some general thoughts.

ad 1. when your experiment is about cognitive control in the wider sense, frontal theta is a very established and reliable EEG marker. But when it comes to frontal EEG asymmetry, I think there is not much established knowledge so far, so it may be worth exploring several frequency bands unless you have clear hypotheses. You should consider doing a current source density transformation, else you may have a hard time detecting asymmetries because of volume conduction effects.

ad 2. if you are looking at frontal asymmetry in response to some events in the VR, it is certainly time-related. You should do a time-frequency analysis instead of computing a mean spectrum for the entire duration of your experiment.

ad 3. The two most common Matlab toolboxes for EEG data analysis are EEGLAB and FieldTrip. Which one you prefer is mainly a matter of personal taste. EEGLAB is easier to learn, since it has a hybrid GUI/script design, whereas FieldTrip is purely script-based. But I guess as a computer scientist, making scripts is not a big challenge for you ;-)

If you need more input, this is an excellent introductory textbook on EEG analysis:

HTH,

Marius

Excellent opinions ...I think all in respect to the general goal behind the question...

Life style changes are also important for migraine management

Nazari, F., Safavi, M., & Mahmudi, M. (2010). Migraine and its relation with lifestyle in women. Pain Practice, 10(3), 228-234.

Good answer Dr Simon N Young!

www.ncbi.nlm.nih.gov/books/NBK21744

Perhaps another way to answer the question is with another question. Did electronic calculators, and subsequently computers, replace mathematicians, accountants, statisticians, and engineers? No. Just made them that much more productive.

Most likely related to a sudden increase in longevevity due to relatively recent technological advances such as the advent of refrigeration and antibiotics that has allowed unrecognized biologically protective genetic factors to become a disadvantage as humans live longer. This genetic factor combined with increased occupational exposures among humans to neurotoxicants which act as disease modifying factors that unmask latent disease earlier is one of the most scientifically plausible explanations. Think about it most other animals have not seen the increase in life expectancy that humans have and they also do not work as pesticide applicators, welders, or miners.

Check out the International Journal of Dream Research, Heidelberg University, Germany, online. (IJoDR)

Hello Mohammed,

In terms of visualizing BBB opening I would recommend these two papers:

I am not familiar with hoesct dyes being used to visualize this, there are many other alternatives like dextrans that are widely used.

I have the same problem...

You can look up Mimetas and easily make a BBB model with their OrganoPlate https://mimetas.com/overview-mimetas-applications/human-blood-brain-barrier

There was a paper published in February this year in Scientific Reports with this platform: https://www.nature.com/articles/s41598-018-20876-2

Hope it helps!

Try to look in Physionet ATM, they already provided many dataset including EEG / ERP studies.

Positivity (positive attitude) leads to the hope of improving the disease and in my opinion it really accelerate the speed of recovery from a disease.

For curing cancer pranayam (breathing practices) and meditation are really beneficial.

Hi Martín,

thanks for your answer, very much appreciated! The nuisance regression is part of my resting state preprocessing pipeline. The overall objective is to submit the cleaned data to a Graph theoretical analysis, in which I compare basically how FC changes in relation to psychopharmacological treatment. So, I had the idea to submit the data to a nuisance regression and write out a new 4D Volume which I then go on to process further.

If I understand it correctly, I could also do the Nuisance Regression in SPM12 as covariates. The ROI to ROI approach is, as far as my understanding goes, a lot easier to conduct with other toolboxes like DPABI or GRETNA.

If you have further advice, I'm very grateful for help!

Best regards,

Pablo

Only one reason in my opinion -- Meniere Spectrum Disorder, or endolymphatic hydrops, a hyperactive condition of the inner ear due in the first instance to reduced perilymph pressure. As with any other mysterious medical condition, the clue is in the associated symptoms. So, if brain fog was a cortical disorder, there should be associated neurological signs/symptoms.

I confidently predict otological symptoms, eg audiosensitivity, vertigo, dizziness, tinnitus, diplacusis, distorted hearing.

A paper has reported that in some few patients, the neurons (or glial cells? see Stereade) seems to be generating delta-like waves (the same frequency than deep sleep) for some hours (?). If that can be replicated, what is happening to the mind? How we should treat a cadaver (smile)?

Hi,

Currently, International Working Group (IWG) and National Institute on Aging Alzheimer's Association (NIA-AA) has proposed several biomarkers as diagnostic criteria which includes cerebro spinal fluid (CSF) amyloid beta (Aβ) and tau, atrophy on MRI, glucose metabolism on [18F]-fluorodeoxyglucose positron emission tomography (FDG-PET) and fibrillar Aβ burden on amyloid PET.

There are few regions, which acts as definite Hallmark regions for AD. You could refer to below attached papers.

Structural MRI and Amyloid PET Imaging for Prediction of Conversion to Alzheimer's Disease in Patients with Mild Cognitive Impairment: A Meta-Analysis

Biomarker-based prediction of progression in MCI: Comparison of AD signature and hippocampal volume with spinal fluid amyloid-β and tau

I hope these article will help you.

Further, regarding the medication you could look into these articles

Drugs for Alzheimer’s Disease: Are They Effective?

Gud Luck !!!!

There are several functional neuroimaging techniques ( e.g. near infrared spectroscopy, EEG, MEG, fMRI and etc) can be used to monitor both physical and mental fatigue. These techniques are chosen for the particular application based on their spatial and temporal resolution and mobility. The following references are for two different studies on fatigue:

[1] K. M. Ranjana and P. Raja, "Effects of Mental Fatigue on the Development of Physical Fatigue: A Neuroergonomic Approach," Human Factors, vol. 56, pp. 645-656, 2014/06/01 2013.

[2] M. Tanaka, A. Ishii, and Y. Watanabe, "Neural effect of physical fatigue on mental fatigue: a magnetoencephalography study," Fatigue: Biomedicine, Health & Behavior, vol. 4, pp. 104-114, 2016.

Surely, the brain's absorption of information is not like feeding data into a computer system, but is dependent upon divisions of memory and the diverse ways that information is embedded? That is through experience (emotional, autobiographical, biographical), accepting and retreiving data, leading to prolonged and complex methods of information inclusion.

Dear Mehrnoosh,

eaA computer memory is like a container of information. The memory is the container, what is remembered are the states of the container. Animal memories are nothing remotly alike a system of holding information. In biology, memory is the actual functioning structure of the organism. Higher animals can change that functioning structure, they can learn new behavior. Human have language, can make behavioral narrative and can even make narrative of some previous events of their life. But most of human memories are like animal memories, implicit and behavioral. Part of our animal memories are visual capacities and part of our explicit memory is also visual. An explicit visual memory is a self-enactment of an implicit visual capacity as are all narrative. Narratives are in all senses and actions modalities. Remembering a particular scene, is a self-enactment of the visual schemata involved when a particular scene was experienced. The visual schemata are part of the visual system and only a small amount of information is needed for the self-enaction of a particular memory, the same happen in dreams.

Here are articles that outline the state of the art. Reading working memory seems feasible. For long term memory one would have to scan synapses. The wavelengths would probably have to be in nanometer range and would therefore be associated with dangerously high energies.

Regards,

Joachim

Tough to say what ever "will be" possible in the future.

As far as current technology can tell, dead people do not emit brain signals, which is part of what defines them as being dead in the first place. There may be some information stored in the brain, like in the hard drive of a computer, which could be "read" with the right technology, but we are nowhere close to doing that yet. We haven't even made it to the point of recognizing thoughts in living people, so I think extracting information from the brains of the dead is something for far, far in the future, if ever.

These are transmission electron micrographs - not the kind of histology appropriate for tissue identification.

The nodose ganglion is outside the skull. The vagus nerve exits the skull thorough a foramen, and the ganglion is very close to this foramen. The round bone above the ganglion is the tympatic bulla.

The brain is 'plastic ' so the neurons will connect to different pathways that will compensate for a lack in another area. Perhaps more connections will be in the temporal lobe instead of occipital lobe

Dear Robert,

Many thanks for your reply.

I am really afraid about the work we may do together if you are available in the lab for only 1 day a week..

but anyway thanks for your interest.

Regards, manish

Hi,

Good luck

I am interested in doing a PhD in Neuroscience. I am a medically qualified person with a MPhil.

There is indeed quite a bit of evidence suggesting that astrocytes can secrete glutamate, however, it is surrounded by much controversy still and there is not a definite consensus on the topic yet. The following papers suggest that glutamate is indeed secreted by astrocytes:

https://www.ncbi.nlm.nih.gov/pubmed/9753099 (1998)

https://www.ncbi.nlm.nih.gov/pubmed/10632596 (2000)

https://www.ncbi.nlm.nih.gov/pubmed/28130845 (2017)

This paper suggests that glial cells can release glutamate by reversal of the glutamate transporter: https://www.ncbi.nlm.nih.gov/pubmed/2247147?dopt=Abstract&holding=npg (1990)

and that this may be important in ischemia: https://www.ncbi.nlm.nih.gov/pubmed/10659851 (2000)

The findings to date are well summarized in the following three reviews:

https://www.ncbi.nlm.nih.gov/pubmed/20300101 (2010)

https://www.ncbi.nlm.nih.gov/pubmed/24559669 (2014)

and most recently: https://www.ncbi.nlm.nih.gov/pubmed/26814587 (2016)

 Hi,

I think you could benefit from this type of work.

All the best,

Mehmet,  MD, PhD

Thank you Dr Joakim and Dr Osama for following my question!

"Yes why Not?"

The question does not make sense.

Frederik A De Wolff 45.02  Leiden University

What is the incidence and mechanism of the excitatory effect of opiates in some humans?

Some patients on opiate or opioid analgesics paradoxically react with hyperactivity, verbosity and insomnia. As a student (more than 50 years ago) this was demonstrated during the pharmacology lectures bij injecting a cat with morphine and show it a white mouse, whereupon the cat panicked and jumped up and down its cage. Our pharmacology professor then explained that 'a small percentage of the human population reacted like cats', and indeed, this is reported incidentally by patients.

Can anybody explain the incidence and mechanism of this paradoxical effect?

What is the incidence and mechanism of the excitatory effect of opiates in some humans?. Available from: https://www.researchgate.net/post/What_is_the_incidence_and_mechanism_of_the_excitatory_effect_of_opiates_in_some_humans [accessed Jun 6, 2017].

 Charles Schaffer & I found evidence that nearly one-third of bipolar patients when taking mu-opiates would have a manic-like reaction that might last a day or two.  In some cases this was the subject[s first manic episode.  There is evidence of interaction between dopamine and opiate system and perhaps a large subset of bipolar patients might be overly sensitive to the DA-opiate interaction.  We published one report but not the second, which had incidence around 35 percent.  Thanks you.Tom Nordahl UCD

Dear Sayam,

Thanks for an interesting question. As many of our colleagues has discussed that dyslipidemia is a modifiable risk factor in the development of dementia and cardiovascular diseases. Mr Sedat has already provided the details of few articles.

Sage, Cardamon and Rosemary, have well documented neuroprotective effects. There are many more.  The research has been done. The fact that these are not patentable substances may have led to less attention being directed towards them.

Here are a few references:

Lopresti AL,  (2017) Salvia (Sage): A Review of its Potential Cognitive-Enhancing and Protective Effects. Drugs In R&D Vol. 17 (1), pp. 53-64.

Masoumi-Ardakani, Y., Mahmoudvand, H.,  Mirzaei, A., Esmaeilpour, K., Hamed, S. Khalifeh, Sepehri, K. (2017). The effect of Elettaria cardamomum extract on anxiety-like behavior in a rat model of post-traumatic stress disorder.  Biomedicine  &  Pharmacotherapy,  87, pp. 489–495.

Park, S., Kim, S., Sapkota.&Kim, S.J. (2010). Neuroprotective Effect of Rosmarinus officinalis Extract on Human Dopaminergic Cell line, SH-SY5Y. Cell Molecular Neurobiology, 30:759–767DOI 10.1007/s10571-010-9502-3

@ Dr Dick Terwel. l am grateful for the pdf you sent. Thanks for your prompt response to my request.

Hi, you can seed astrocytes or pericytes ( I use ~ 50ul containing 50,000 cells) on the outer side of the coated inserts kept in a 20 cm dish. Transfer this carefully to incubator. These cells should attach quickly in around 2 hours. Then you invert the insert, keep in a 24 well plate and seed endothelial cells. 

Thank you Dr Josep & Dr Jordi

Since you have elected to respond with alacrity (as if we are in a fencing match) without much reflection on a miniscule of what was written, and you are obviously enthralled by your own hypothesis, please also let us know how nausea and vomiting of pvd (if, as it seems, migraine must be due to pvd), resolves the headache of migraine in a sizable fraction of migraineurs--a finding noted by Hippocrates but ignored by scientists of the twentieth and the twenty-first century. A pinch of salt "may" help in many medical disorders, and if Google is to replace systematic in-depth medical research and commentary, God help humanity. Like Watson and Crick, a colleague who can dampen over-enthusiasm and acknowledge error is invaluable--simply because humans find it very difficult if not impossible to acknowledge errors or limitations. Dear Anthony, let the world remain flat. I rest the case and accept your version of the "truth".

Thanks a lot, Dr. Develi.

I already read these review articles. However, these were not very conclusive about the role of glutamate from imaging point of view. 

However, migraine community seems to strongly believe in the key role of glutamate in migraine. I would like to know what are the arguments and evidence in its favor?

I don't think I can add anything more, other than to recommend Luria's work on the functional systems in the brain.   The antireductionist literature is like wading through mud, and is largely wishful thinking.     

may be ,but in humans more complex , but in the animals specially rodent its an visible.( I  think)  

Dear Dr Anter, 

Thanks so much for the link. However, I could not find what I was looking for.

In fact, I was looking for some MR datasets for patients where each patient has multiple scans with time period being known between the scans.

Unfortunately, the link you have provided does not have such datasets.

Anyway, thanks so much and have a nice day.

Hi!

I think the best way to normalize is to take the fft both on baseline and on the trials.

Then, you should whiten the power spectra to avoid pink-noise of the brain. (whitening means that you multiply the power value in the given frequency with the given frequency).

After that you can divide your power-spectra of the trials and the baseline into chossen frequency bands. Althought it's not compulsory, if you would like to interpret your results in each frequency, it's ok.

So, you have the whitened power spectra in the given frequency (or frequency band) of trials (Pt) and the baseline (Pb). You can then normalize them in each frequency in two ways: logarythmic and percentile-way. I will show you the percentle-way:

N=100+100*(mean(Pb)-mean(Pt)/mean(Pb))

This will give you the percentile-changes compared to the baseline. N=100 means that Pb was equal to Pt (no changes occured, N=200 means that Pt was 2*Pb.

Also, make sure that the length of baseline and the trilas are equal in order to avoid mismatches of the frequency resolution of the power-spectra. (If they aren't equal, make sure that you calculated the frequency resolution properly) 

You can find pretty good lecturelets here: http://mikexcohen.com/lectures.html, and I reccomend Cohen's book (https://www.amazon.com/Analyzing-Neural-Time-Series-Data/dp/0262019876/)  if you would like to work with EEG-analysis.

Hope I helped!

András Puszta MD

Pinnacle’s THREE-CHANNEL TETHERED MOUSE SYSTEM allows researchers to simultaneously record three channels of EEG and/or EMG data. The data conditioning and acquisition system (DCAS) and preamplifier are preconfigured and ordered as a matching pair. Fully independent preamplifiers are also available.

 This article may be of help: SEIZURE ACTIVITY INVOLVED IN THE UP-REGULATION OF BDNF mRNA EXPRESSION BY ACTIVATION OF CENTRAL MU OPIOID RECEPTORS

H. N. ZHANG and M. C. KO Neuroscience. 2009 Jun 16; 161(1): 301–310

Thank you both. very helpful

Also, you can check Paxinos' textbook. (For Rats)

George Paxinos, Charles Watson The Rat Brain in Stereotaxic Coordinates

There are a number of causes for transient hyperintensity on CT, like blood and intravascular thrombosis. Sometimes elevated pressure or focal edema may falsely cause parts of the brain appear hyperdense. If I remember correctly, transient CT hyperintensities have been observed in status epilepticus. On the other hand, I have seen hundreds of CT scans of patients with focal encephalitis - some with status epilepticus - in whom the CT finding was always a hypodensity and/or expansion, hemorrhage, or nothing at all. What you describe is probably a rare phenomenon and might even be worth reporting. Do not get discouraged by the fact that a ton of transient this and thats on MRI have been published.

BTW, did you take video of the chorea?

i have uploaded the MRI to this link

Thank you so much Dr. Aldallal,

for sure this paper contain very useful information, 

Tests that measure the sense of smell may soon become common in neurologists' offices. Scientists have been finding increasing evidence that the sense of smell declines sharply in the early stages of Alzheimer's, and now a new study from the Perelman School of Medicine at the University of Pennsylvania published today in the Journal of Alzheimer's Disease confirms that administering a simple "sniff test" can enhance the accuracy of diagnosing this dreaded disease.

The sniff test also appears to be useful for diagnosing a pre-dementia condition called mild cognitive impairment (MCI), which often progresses to Alzheimer's dementia within a few years.

Neurologists have been eager to find new ways to identify people who are at high risk of Alzheimer's dementia but do not yet show any symptoms. There is a widespread consensus that Alzheimer's medications now under development may not work after dementia has set in.

"There's the exciting possibility here that a decline in the sense of smell can be used to identify people at risk years before they develop dementia," said principal investigator David R. Roalf, PhD, an assistant professor in the department of Psychiatry at Penn.

Roalf and his colleagues used a simple, commercially available test known as the Sniffin' Sticks Odor Identification Test, in which subjects must try to identify 16 different odors. They administered the sniff test, and a standard cognitive test (the Montreal Cognitive Assessment), to 728 elderly people.

The subjects had already been evaluated by doctors at Penn with an array of neurological methods, and according to expert consensus had been placed in one of three categories: "healthy older adult," "mild cognitive impairment," or "Alzheimer's dementia." Roalf and his team used the results from the cognitive test alone, or combined with the sniff test, to see how well they identified subjects in each category.

In my opinion this is a good base to get an idea.

If you acquire very high resolution data, and at the correct b-value, then this should be possible. I would suggest using a technique for selective k-space - GE calls this FOCUS, Siemens call it ZoomIt - to acquire a limited FOV in k-space and therefore very high resolution. I would suggest using this technique to acquire something around 0.5mm (500 micron) resolution with at least 2 averages. Your radiographer will suggest the best b-value, but I would try somewhere between 300 and 500. You shouldn't need to acquire many diffusion directions (I think 25 would be sufficient).

Jerome

I agree with Shafagat Mahmudova good references. thanks

Dear marek.

In my project about traumatic brain injury amantadine also used for the positive control group..

Yes, this is an interesting article. Thanks for sharing.

This article was about increasing parkin activity, you can check it: Ubiquitination Increases Parkin Activity to Promote Autophagic α Synuclein Clearance - Plos journals.

The papers I saw explained about 1% for general antibodies. With the dysfunction of the BBB, it may go up a few %. But remember that Abeta is in decent levels in the blood and these antibodies will likely bind targets in the blood first...

Hello,

Here is a recently published article

NeuroRehabilitation. 2016 Jun 18;39(1):135-40. doi: 10.3233/NRE-161345.

Effectiveness of Animal Assisted Therapy after brain injury: A bridge to improved outcomes in CRT.

Stapleton M.