Science topic

Brain Diseases - Science topic

Pathologic conditions affecting the BRAIN, which is composed of the intracranial components of the CENTRAL NERVOUS SYSTEM. This includes (but is not limited to) the CEREBRAL CORTEX; intracranial white matter; BASAL GANGLIA; THALAMUS; HYPOTHALAMUS; BRAIN STEM; and CEREBELLUM.
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How Does COVID-19 Affect the Brain? Are there implications of COVID-19 in Neurological Disorders?
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Sure, COVID 19 can affect the brain. As we saw in our practice many patients with covid 19 had ischemic stroke, Encephalopathy. also I have 2 patients , the presenting features of coved 19 were Polymyositis, and 3 patients with GBS.
many individuals had post covid ischemic stroke
Thanks
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It is well known that Doose and Lennox-Gastaut syndromes are drug resistant epileptic encephalopathies. There do exist typical AED for them. Nevertheless, although AED as
carbamazepine is not recommended -as a result of the many possible side effects it may cause- does there exist any report about any child/adult which was in good control of seizures with levetiracetam, etosuximide, topiramate, lamotrigone and clobazam and - in order to "increase seizure control" those AED are retired slowly, levetiracetam is changed by brivaracetam BUT CARBAMAZEPINE is introduced as "the new one" and is suppported by risperidone...?
I will acknowledge any comment.
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Dear Ricardo
To the best of my knowledge, there are no data about a possible increase of early death rate in LGS patients treated with CBZ.
Anyway, LGS has an increased risk of early death, especially in patients with high seizure rate (DOI: 10.1177/0883073809348355). CBZ can exacerbate seizures in LGS, especially tonic seizures (frequent during sleep).
I can argue that this might increase the risk factors for early death in selected LGS patients.
Bw
Elena Gardella
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The association of free radicals in the pathophysiology of chronic diseases like degenerative brain disorders (AD, PD, HD, Stroke) has been evident by a substantial research.
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Limbic-predominant age-related TDP-43 encephalopathy (LATE) is a quite hot topic these days among those who are concerned with dementia, memory deficits and neurodegenerative diseases.
It has been suggested that LATE is distinguished from frontotemporal lobar degeneration (FTLD) with TDP-43 pathology based on its epidemiology.
What do you think about this newly recognized disease?
Any idea about the potential or promising diagnostic approaches?
Possible future biomarkers and mechanisms...
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There is a nice article in Nature Neuroscience 2019;22:65-77.... "TDP-43 extracted from FTD brains displays distinct aggregate assemblies and neurotoxic effects."
They showed that FTD-TDP type A patients were more likely to manifest signs of behavioral variant FTD, and that FTD-TDP type B patients were more likely to manifest signs of the motor neuron variant of FTD, while the FTD-TDP type C patients showed signs of semantic dementia.
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05 months old child .
rare brain diseases.
my reading is .
megalencephalic leukodystrophy DDX Canavans, Alaxanders.
any body with expertise in pediatric neuro radiology to help me with this patient.
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Thank you for the input
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Please write to me and give some info about yourself. The reviews are going to be published in Q1 journals.
Cheers
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Count on me, let me know what you would like to have from me. Best
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The blood–brain barrier is composed of high-density cells restricting passage of substances from the bloodstream much more than do the endothelial cells in capillaries elsewhere in the body. over 95 percent of drugs do not show any useful activity in the brain due to the blood–brain barrier. therefor opening them for a short while can be very effective.
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Hi Maryam, if you want to open the BBB to allow drugs to cross it and diffuse in the brain, then ultra-sound and microbubbles. It is used in various preclinical studies and even in human for cancer therapy and now for Alzheimer's disease:
Here is what was done in my previous lab for preclinical studies:
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Hello everyone,
Epilepsy is a chronic brain disorder characterized by recurrent seizures. Globally, 50 million people around the world live with it, while ,annually, a rate of 2.5 million new case is diagnosed to have it.
Unfortunately, one-third of the cases had shown a resistance to the Anti-Epileptic Drugs(AEDs) being prescribed for them by the physician. In these cases, the surgical intervention becomes a must. So we need to precisely localize the region involved in this disease and asses the eligibility of the patient for such surgery.
Many functional neuroimaging techniques have been used in order to perform such kind of assesment (such as MRI, PET,SPECT, etc.) but these methods provide a low temporal resolution which is needed for transient events such as the spikes. While the EEG method can provide a high temporal resolution. Hence, Many researches have been conducted on how to use the EEG along side the signal processing techniques to provide a better understanding of the spatio-temporal activity in the brain (solving the inverse problem).
I am interested in time varying source localization. So kindly, can any one of you suggest some literature review related to this issue?
Thank you in advance.
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Hello Sajidah,
you may wish to review literature on application of eLoreta algorithm based software electroencephalograph with Dynamic Electrical Cortical Imaging . please see below relevant link on this technology:
Kind regards,
tatyana
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Postop craniotomy and AVM malformation. Discussing the safety of Ketoroloc for pain control in postoperative period in this patient population  
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W. Jerry Oakes has published a study on this question years ago in Pediatric Neurosurgery literature.
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I am performing western blot analysis to detect the protein expression changes in the brain tissues from several neurodegenerative diseases (e.g Alzheimer's, Parkinson's) as compared to normal control (age-matched). In your experience, which is a better loading control - GAPDH, ßActin or α/ßTubulin?
If you are aware of any articles that addresses above question, please do share.
Thank you for your feedback!!
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Hi,
The journal of biological chemistry (JBC) declares in the editorial recommendations that "Normalize signal intensity to total protein loading (assessed by staining membranes for total protein) whenever possible. “House-keeping” proteins should not be used for normalization without evidence that manipulations do not affect expression.".
For more information the JBC indicates:
Interestingly, Dr Oh informs that journals often openly state that of the western blotting normalization methods they prefer, total protein techniques are at the top of the list. In fact, since 2012 when it was first introduced, stain-free total normalization has appeared in over 800 publications (almost 500 of those appearing in 2017).
For more information
I suggest as total protein quantification method the membrane staining with Ponceau S., Coomassie Blue or Amido black.
Best regards.
Mauricio
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Need to apply life-cycle asset management approaches to enhance sports engineering. Like infrastructure, the human body has an 80-year+ life-span - which is why we go to the dentist and have regular check-ups. Preventive maintenance, proservation techniques, life-cycle value engineering can all play into the sports engineering field. Sports engineering has the $$$ incentive to produce great results in longevity of life spans. Look how the results of war have contributed to human reconstruction. Sports madicen can also benefit from sports engineering - consider the extension to robotics.
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I know Rick Greenwald from Simbex has been extensively working on monitoring impacts on helmets to try to prevent concussion.
Hope that can help
Thomas
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In the March 5 update of the project "Prescriptive ontology in the Hebrew Bible", the resonant interaction of a number N of two level systems (TLS) in a cavity with an electro-magnetic field at a cavity mode frequency was discussed . When the transitions from the lower to the upper level of the TLS are in phase, the interaction energy is largest and the in phase oscillating system is the polariton Bose-Einstein condensate. It can occur at ambient temperature because it is stabilized by the matter-field interaction, which occurs in the strongly coupled, robust, pumped polariton condensates but not in systems composed of matter alone, such as the fragile Fröhlich condensates . At high interaction energies, optics becomes non-linear, The TLS oscillates between the upper state and the lower state at the Rabi frequency, by emission and re-absorption of resonant photons. The Rabi frequency is equal to the light- TLS interaction energy of the Bose-Einstein condensate divided by Planck's constant.
In microtubules, at the cavity mode resonance, the interaction energy of the polariton condensate is largest, not only because of the large Rabi frequency but also because of the strong induced dipole-dipole interaction between tubulin rings. This leads to an interesting polariton-condensation-induced chemical effect: the increase of the length of the microtubule molecule by polymerization of tubulin. The maximum effect of microtubule lengthening is obtained at the electromagnetic field frequency which resonates with the cavity mode frequency. Changing the cavity dimensions will change the electromagnetic field frequency producing maximum microtubule lengthening. Electromagnetically-induced polymerization of neuron tubulin in a cavity was obtained in 2014 by Bandyopadhyay et al, without noticing that thereby they introduced polariton chemistry; see https://www.nature.com/articles/srep07303.pdf This discovery can lead to new treatments of Parkinson's disease and other brain disorders, as was noted by Stuart Hameroff in his YouTube presentations.
The question presented here is whether cavity polariton polymerization is a general mechanism in biology.
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The cell membrane potential is caused by a plasma formed by negative charges on the inside of the membrane and positive charges on its outside. Presumablym this increases reflection of electro-magnetic waves in the cell cavity and improves the Q-factor for cavity polariton polymerization in the cell. This mechanism may be the explanation of the origin of life.
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Is there any process by which we can detect early stages of Alzheimer?
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Back home, they say if someone can't find his car key (forgot where he put it) this will be the first sign.
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review article needed foe machine learning approaches to detect brain disoredr
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Dear Sohail,
Please refer to the followings:
Insel, T., Cuthbert, B., Garvey, M., Heinssen, R., Pine, D. S., Quinn, K., ... & Wang, P. (2010). Research domain criteria (RDoC): toward a new classification framework for research on mental disorders.
El-Dahshan, E. S. A., Mohsen, H. M., Revett, K., & Salem, A. B. M. (2014). Computer-aided diagnosis of human brain tumor through MRI: A survey and a new algorithm. Expert systems with Applications, 41(11), 5526-5545.
Gaiteri, C., Ding, Y., French, B., Tseng, G. C., & Sibille, E. (2014). Beyond modules and hubs: the potential of gene coexpression networks for investigating molecular mechanisms of complex brain disorders. Genes, Brain and Behavior, 13(1), 13-24.
Dwyer, D. B., Falkai, P., & Koutsouleris, N. (2018). Machine Learning Approaches for Clinical Psychology and Psychiatry. Annual Review of Clinical Psychology, (0).
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the recent researches have shown that blind people react(smile) to the smile of a person in front of them. how this connection occures?
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Professor Zeashan Khan,
Thank you very much.
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Optogenetics is branch of biotechnology, which is growing and emerging in the treatment of many brain diseases including depression, Parkinson, so what are new innovations related to obesity and diabetes.
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Optogenetics is an emerging field that uses light-sensitive proteins to regulate biological activities in the body. The technique has been envisioned as a way to treat a range of diseases, including Parkinson’s and schizophrenia.
Optogenetics to precisely control cells to deliver insulin to diabetic patient. The approach could be used to continuously monitor blood glucose levels in human diabetics and automatically produce necessary insulin, a hormone that converts sugar from food into energy the body can use.
The researchers engineered human cells with a light-sensitive gene that is found in plants and produces insulin on cue when activated by wirelessly powered red LED lights. They inserted those lights and the designer cells onto small, flexible discs that were then grafted onto the backs of person or any place of the body.
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A recent landmark Nature paper (attached) following up on a cohort of congenital toxoplasmosis since 1981, has described the association between Toxoplasmosis infection and certain degenerative brain disease. Baring in mind that the studied cohort does not represent the population at large, would you consider Toxoplasmosis testing in an adult with degenrative brain disease (E.g Parkinson's, Alzeheimer's...)
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Zipurshy RB, Reilly TJ, Murray RM. The myth of schizophrenia as a progressive brain disease. Schizophr Bull 2013;39:1363-72
Andreasen NC, Liu D, Ziebell S, et al. Relapse duration, treatment intensity, and brain tissue loss in schizophrenia: a prospective longitudinal MRI study. Am J Psychiatry 2013; 170:609-15
Dorph-Petersen KA, Pierri JN, Perel JM, et al. The influence of chronic exposure to antipsychotic medications on brain size before and after tissue fixation: a comparison of haloperidol and olanzapine in macaque monkeys. Neuropsychopharmacology 2005;30:1649-61
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Dear Giacinto
Antipsychotics are not addictive as are drugs like cocaine, narcotics, benzodiazepine, alcohol. People with schizophrenia usually don't want to take them and stop taking them without withdrawal side effects or developing a craving for them.
Antipsychotics do have a street value in some places. A lot of people abuse painkillers such as paracetamol, not because they are in pain or that they are trying to harm themselves, but that it makes them feel good. Paracetamol is hardly described as addictive. A lot of people love and eat too much chocolate, is that an addiction?. I myself love and eat a lot of fish, am I addicted to fish?
Antipsychotics are probabely as "addictive" as paracetamol, chocolate and fish, but are hardly in the same category of addiction as cocaine, narcotics, benzodiazepine, alcohol.
As to whether schizophrenia exists or not:
What should we call that state where a group of people usually from an early age start to think strange things ( by the standards of an average person) and which have come to be defined "delusions" or that the order of their thoughts gets disrupted (come to be defined as "thought disorder"), start to hear voices (come to be defined as "auditory hallucinations").
And what should society do with these unfortunate people if anything?
When Loren Mosher started his career was Loren not aware that he will have to be dealing with antipsychotic drugs or what his job role would be? What alternatives did he have to offer?
There is still a lot of uncertainties in mental health but this is so in many other fields.
Software is released with the full knowledge that it still contains "bugs" which will need to be fixed later.
The aeroplanes of the 1960's were not as safe as they are now. Even the aeroplanes of today are not 100% safe, they still crash. It is by a process of iteration that improvements are made . We do not need a complete understanding of a problem, before we try to do anything about it. We still fly incompletely safe planes and release software with "bugs" in.
One solution to schizophrenia is antipsychotics and psycho-education (according to the current paradigm).
What is the alternative solution suggested by those who doubt this (and what is the evidence for these alternatives) especially for those who are not happy with their delusions and hallucinations and are suffering massively being driven to suicide for instance?
You state about antipsychotics that:
"It is certain that they involve deep changes in brain function, they are addictive and, above all, difficult to suspend, at the cost of coming back of an increased form of symptoms, often mistaken with a relapse of the disease."
You state about schizophrenia (about which you are not sure whether it exists) that:
"It is a useless operation if we think that schizophrenia is a biological disorder and its symptoms are only something to be attacked and eliminated."
This means that when drugs that act on the brain, about which you do agree, are stopped the "symptoms" come back. How is that possible if schizophrenia has nothing to do with the brain and is not a biological disorder and these drugs do act on the brain and work biologically.  Is it a side effect of these drugs that they get rid of the symptoms, by acting on some other organ and what organ is this? But if they do that they are still acting biologically. How can these agents that affect biology affect a non biological condition? On the other hand, applying Occams Razor the conclusion is that schizophrenia is a neurobiological condition affected by agents that act on the neurobiology.
How do you explain that the symptoms of a non biological condition get worse when these biology altering agents are stopped?
That it is unwise to accept that schizophrenia is a condition that does exist, that it is unwise to accept that it is a brain disorder, that it is unwise to accept that it can be treated by antipsychotics will require a lot of proof that obeys the rules of logic in order to bring about a paradigm shift away from the current. Paradigm shifts have happened before when insulin comma therapy was abolished, thalidomide was withdrawn, sertindole was withdrawn, use of leeches were withdrawn etc.
Doubters of the current schizophrenia paradigm need to bring about a paradigm shift with evidence  that follows the rules of logic in order to get their paradigm accepted by all.
Please see
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I am designing an automatic diagnosis system for detecting some brain diseases like Epilepsy,Alzheimer's and sleep disorders like Insomnia,Narcolepsy. But the problem is the features I have extracted are giving values in the same range for two diseases. So individually if I detect a single disease for my test EEG signal then it is showing positive for two disease. How can we solve this problem. Can we design a single system for all diseases rather than one system for each diseas.
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Although probably not what you looking for, simple physiological variables might add clarity such as age, EMG, HRV, BMI, reaction time, ...  I think the approach of looking for a number of diseases and trying to access their probabilities and distinguish from healthy controls may prove fruitful. Also the diseases that you mention have co-morbidities.  The  disease descriptions are inherently symptomatic and not based upon brain/body structure (just because we do not have the diagnostic ability to do so).  The results that you are getting may be accurate.  It is just that the diseases overlap.  Ultimately, this is a combine sensor and big data problem.
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Clinical biochemistry
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I want to do a research about the the protecting fuction of Nuclear factor-erythroid 2-related factor 2 (Nrf2) in ischemia brain disease.
However, I do not konw what kind of Nrf2 activator and inhibitor we always use?
Can they pass through blood brain barrier and regulating the Nrf2 protein level of brain tissues?
Would you mind telling me which article is the most authoritative one?
Thanks for your great answer!
              A new comer of ischemia brain disease.
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This is one of the inhibitor of keap1-Nrf2 interaction. There are several of them. But this has good computational and in vitro results. Hope that helps. MG
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I am working on a family with autosomal recessive in which affected members have CP characters so how will i differentiate between whether it is Cerebral Palsy or Heredity Spastic Paraplegia?
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Maybe you have to try out the old clinical practice: do longitudinal observation: CP usually remains stationary, given adaptive changes after birth; HSP should be slowly progressive with an later onset. Still, it remains a big challenge for a clinician to tackle the differences.
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i need a list of inducer that can Alzheimer like symptoms....other than heavy metals and stress inducer???
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Let me first apologize for putting this collaboration request in question-answer section. However, I could think of any other way to reach to relevant researchers faster.
I am an MRI scientist working at the dept. of Neuroradiology, University Medical Center, Hamburg. 
I have been working towards making T2-relaxometry based myelin imaging as a feasible clinical (MRI) marker. For that, I am using the gold standard CPMG sequence and exploring ways to cut down the scan time for whole brain coverage  < 15-20 minutes using various regular and random under sampling (compressed sensing). 
I am planning to apply for an international collaboration grant between India-EU. This grant aims to make collaboration between India and following EU countries: Belgium, Estonia, Portugal, France and Norway. More information here: http://indigoprojects.eu/funding/indigo-calls/call-2015
I am looking for collaborators (from India/ Belgium, Estonia, Portugal, France and Norway):
1)    who is interested in white matter disorders: It could be any white matter disease.
2)     who may have following backgrounds:
a.      Sequence development
b.      Compressed sensing
c.       Medical background
d.       Histological background 
Any interested MRI/ “white matter disorder” researcher can contact me:
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Thanks, Ashutosh. However, the collaboration must be with researchers from:  India & Belgium, Estonia, Portugal, France and Norway.
None the less, I would really be interested in collaborating with him/ his PhD supervisor, since I am interested in myelination of central nervous system; but, from imaging point of view. Possible collaborating and joint funding proposal is very much possible.
Could you please introduce me to him?
My email id is: (dushyantkumar1) (AT)(gmail.com)