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Parkinson's Disease - Science topic

A topic to discuss Parkinson's disease research: Basic science, clinical research, treatment.
Questions related to Parkinson's Disease
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Dear Researchers,
What is the best way to deal with imbalanced Dataset when the Imbalanced ratio , IR is more than 4.5 (majority 2000, minority 400) ? If I want to use deep learning methods or transfer learning for classification, what is the best way to augment the data. In my problem Healthy control dataset is the minority.
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Understand the common techniques like Over Sampling, Under Sampling, generate synthetic data to handle imbalanced datasets, and finally, apply all the concepts to an imbalanced dataset. An imbalanced dataset is one in which one class has disproportionate observations compared to the other classes.
The correct use of the k-fold cross-validation in an imbalanced class distribution problem, require: That each k-fold data is stratified to capture the imbalanced class distribution of the target feature in the main data. This can be achieved using the stratified k-fold cross-validation;
GOOD LUCK
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Hello everyone! I am curious as to whether we can induce mitophagy in HEK293T (or HEK293, which should be similar?) cells, without Parkin transfection?
I have read some papers in the mitophagy field and got an impression that many of them use HeLa cells, which don't express Parkin endogenously, as the model cell line to study mitophagy. For mitophagy induction, they needed to transfect Parkin into the cells and exert chemical treatments afterward. And I was confused why they use HeLa cells to begin with.
If anyone has had success in studying Parkin/Pink1 mitophagy in HEK293T cells, could I get some advice as to what chemicals you use and the duration of the treatment to induce mitophagy? Thanks very much!
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I am also curious about your work. I am trying SH-SY5Y mitophagy via AAV transduction and siRNA-induced knockdown of Parkin?
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I start learning about synchronization between different states and criticality in Parkinson's disease. Would it be possible for someone to recommend a relevant and practical review paper that examines the new challenges arising in this field?
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Dear Sheida,
Here, we discussed the role of cortico-subcortical circuits in the emergence of abnormal beta oscillations as well as abnormal synchronization in PD:
The relation between patterned neural activity and abnormal synchronization in PD is briefly discussed here:
A reference review article can be found here:
Also, take a look at:
Good luck,
Best regards,
Mojtaba
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I am working on EEG self-detection of Parkinson's disease and I would need to apply my methods on data from people with Parkinson's disease subjected to ERPs or ssEVPs with a control group of healthy people subjected to the same stimulation under the same conditions.
I have been searching for a year without being able to find a database. So I am looking for a direct link to a laboratory or researcher who can provide me with this data.
Thank you.
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Hi,
See this site, it may help you:
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Parkinson Disease (PD) is a degenerative disease that affects motor function and sequential.
At which level of H&Y stages will this improve?
Short term or long term effect?
Any evidence to help patient and client?
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Hi everyone,
I have been having some issues with SHSY5Y cells that I never had in the past. I used to culture them in DMEM:F12 with 10% FBS and 1%Antibiotic-Antimycotic and they grew just fine. Back in October, when we received a new batch of medium, I started seeing increased cell death after 1-2 passages: specifically, I would see debris like structures and the cells literally peeling off from the bottom of the flask. I initially attributed this to the quality of the medium and ruled out incubator, FBS etc issues. I thawed a new vial of cells and I had the same issue. Then I was told to try OptiMEM and with a new vial from ATCC I noticed that they grew beautifully and reached confluence within 3 days. After the 3rd passage, I started seeing the same type of pattern that I saw before--cells fragmenting, a lot of debris and cells peeling off and floating in suspension 1-2 days after plating. I am desperate as my lab has wasted many cell stocks and money on trying to figure out what this is. My next step is to test for mycoplasma but I wasn't sure if this is the case considering that we literally just bought a new stock from ATCC and it grew fine until the third passage.The medium doesn't yellow out and it is not yeast contamination. What can be the source of this type of behavior?Any input is greatly appreciated! :)
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I tried a different incubator as well but only after i noticed cell drath. I will thaw a new vial of cells and start from scratch with a new incubator.
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I'm studying with a-syn preformed fibril for obtaining Parkinson's Disease model in rodents. We are trying to probe-sonicate the fibril at room temperature using different settings to obtain a fibril fragment within 40-50 nm. So, we tried to adapt your protocol (Generation of Alpha-synuclein Preformed Fibrils from Monomers and Use In Vivo) for our sonication trials; however, we couldn't reach the desired smaller diameter.
Details of our trials:
Trial 1: We used 20-25% amplitude (power of our sonicator 70W and diameter of probe is 3 mm), total 30 sec (1 sec on, 1 sec off) for 5ug/ul PFF solution, but according to the zetasizer result, we obtained fibril fragments of 505 nm average size. In the second step, we extended the time, making it 2 minute. But again, the fibril fragments were average 930 nm. Finally, we diluted the solution to 2 ug/ul from 5 ug/ul, we tried %20-25 amplitude (power of our sonicator 70W), total 60 sec (1 sec on, 1 sec off). Zetasizer results were 470 nm average size.
We thought our sonicator is weaker than in the protocol, so we tried to use more powerful a sonicator than previous at trial 2.
Trial 2: We used %30 amplitude (power of our sonicator 500W and diameter of probe is 2 mm), total 60 sec (1 sec on, 1 sec off) in 5 ug/ul and 2 ug/ul PFF solution. Zetasizer results were 549 nm average size. After then, we continued to sonicate for 2 more minutes (the total 3 minute – 1 sec on 1 sec off). Measurement results were 918 nm as average.
If possible, could you provide us with any suggestions to sonicate the fibrils?
Thanks for your helps.
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Hi, i work with fibrils in rats. Our labs and others have found that probe tip sonication is less efficient than water bath sonication at obtaining smaller fragments. With probe tip sonicators you can sonicate only for so long before you run the risk of over heating the sample. For more detail please seek out published protocols and also a best practices paper by Laura Volpicelli-Daley.
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8 µg (in 1.6 µL) of 6-OHDA was introduced into the right striatum of mice according to the coordinates A = 0.5, L = 2.0, and V = -3.5 relative to bregma. The needle was withdrawn 5 min after the injection. Seven days after operation, 0.5 mg / kg apomorphine was used to induce rotation, Unfortunately, only a few mice were able to induce seven rotations per minute. Can someone please tell me what went wrong? How can I improve the surgical or experimental protocol?
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Did you verify surgical location? You should verify canula placement prior to behavioral testing. Then again after the experiment, you need to verify placement and the effectiveness of the lesion. Stain for a marker of dopaminergic phenotype.
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Hi, I am going to conduct online research on effect of physical activity in Parkinson disease patients. So for that reason I need help with questions.
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Hello, Shin Murakami . There are several tools that have already been developed and validated so I suggest you use one of those. Here's a good review article with many relevant references for you to check out.
Helmerhorst HJ, Brage S, Warren J, Besson H, Ekelund U. A systematic review of reliability and objective criterion-related validity of physical activity questionnaires. Int J Behav Nutr Phys Act. 2012;9:103.
Best of luck to you!
Brooke
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We have published today a paper at Springer Nature journal of Scientific Reports entitled "Optimal time lags from causal prediction model help stratify and forecast nervous system pathology" by Theodoros Bermperidis and co-authors from my lab at Rutgers, colleagues at Stevens Institute of Technology and Columbia University. The paper describes how to standardize signals from wearables and make causal predictions forecasting disorders of genetic origins and unknown etiology. These included Fragile X and SHANK3 deletion syndromes, both linked to Autism, and Parkinson's disease and Vestibular Dizziness Handicap. I wonder if we could use gait more often in the clinical settings now that we have off-the-shelf wearables at our disposal. Research shows that it would improve classification and help stratify heterogeneous disorders like Autism and Parkinson's disease. Read more here https://www.nature.com/articles/s41598-021-00156-2
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Excellent, Elizabeth. Congratulations on this groundbreaking contribution.
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I see that many papers include analyzing calcium in their methods when the differentiation of iPSCs to neurons is taking place. Why is this necessary?
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Basal calcium is usually low in the cytoplasm of unstimulated cells, most of it is stored in the ER and in the extracellular environment. A good way to assess the differentiation of iPSCs to neurons is by testing their ability to respond to external stimuli or to fire spontaneously after synapse formation in culture. These activities would determine calcium transients that can be measured and quantified - e.g. comparing the response to the baseline (stimulus vs absence of stimulus). You can check this paper about an iPSCs-derived disease model.
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Conversely, rotenone, which is an insecticide, has.
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in fly model MPTP can be used to induce parkinsons disease refer the following article for further clarification.
"Resveratrol prolongs lifespan and improves 1-methyl-4-phenyl1,2,3,6-tetrahydropyridine-induced oxidative damage and behavioural deficits in Drosophila melanogaster"
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Adverse health effects from Rotenone have been well documented in the time since the NOSB reviewed botanicals in 1994. But still Rotenone is continue to be used for organic production. Although no longer offered for sale in the USA, rotenone is still in use as a pesticide on organic farms. Among the compelling reasons to prohibit rotenone, the most heavy is it's linked to eye problems and Parkinson's disease. Astornishelly enough is to note that Rotenone's synergist, piperonyl butoxide, is prohibited from use in organic agriculture.
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Dr. Tsyrlov, I found your question interesting. I found that rotenone is associated with the induction of parkinsonism in rat models. Also, ''Rotenone will be added as a nonsynthetic substances prohibited for use in organic crop production.'' https://www.jdsupra.com/legalnews/usda-amends-the-national-list-of-54211/
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How to make a Parkinson's disease (PD) model of Zebrafish ?
Is there any detail protocol ?
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Hi Achmad,
There are also MPTP models. Simply google "MPTP Zebrafish" and you'll find several papers using the drug model.
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I am trying to figure out how to differentiate between the pars compacta and pars reticulata. In healthy patients you can easily see the difference between the both where pars compacta has a lot of dopaminergic cells and pars reticulata doesn't. However when I look at the SN of Parkinson's patients, the clear/obvious/visible border isn't there anymore. The cells in the Substantia Nigra pars compacta (especially the ventral group, so closest to the pars reticulata) are degenerated. Thus, the clear border is gone. I am not sure where the pars compacta stops now and where the pars reticulata starts.
Are there more hallmarks to define the border between the pars compacta and reticulata?
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Hi Lydian,
We have used morphometry to distinguish between pars reticula and compacta, verified by regional analysis using a steriotaxic atlas, in rodents! Whilst we have done some of this work in non-human primates, similar work in humans brain is sadly, very limited. The key may be to use, if you guys are set up for it, multiple labeling immunofluorescence (as suggested by Max), possibly backed up by morphometric analysis. I have added a manuscript which may be useful. Wish you the best!
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Is the motor complications in Parkinson's disease are due to early use of L-Dopa or due to progression of the disease
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Extended use of levodopa can result in the patient experiencing dyskinesia (involuntary movements) and motor fluctuations (where the patient experiences “off-time” periods, as the drug, wears off and symptoms re-emerge).
Also, Parkinson diseases are progressive diseases
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Hello! I'm a Physical Therapy student and currently working on research about stabilizing spoons and their effects on people with PD and ET. I was hoping that some of you may have known any systematic review or RCT articles that I could use as a reference for my study?
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Hello Maria! These recent articles could be a starting point for your research. The first article is available in open access. The second is a conference paper available in full-text on this platform.
1. Lauren, E. R., Elie, M., Jennifer, Y. Y. S., Deborah, A. H., Paul, C., & Simon, J. G. L. (2020). Shaken not stirred: a pilot study testing a gyroscopic spoon stabilization device in parkinson's disease and tremor. Annals of Indian Academy of Neurology, 23(3), 409–411. https://doi.org/10.4103/aian.AIAN_251_19
2. Turgeon, P., Laliberte, T., Routhier, F., Campeau-Lecours, A., & 2019 IEEE 16th International Conference on Rehabilitation Robotics (ICORR) Toronto, ON, Canada 2019 June 24 - 2019 June 28. (2019). IEEE 16th international conference on rehabilitation robotics (icorr). In Preliminary design of an active stabilization assistive eating device for people living with movement disorders(pp. 217–223). essay, IEEE. https://doi.org/10.1109/ICORR.2019.8779388
If you are looking for high-quality studies, a look in the Cochrane Library may be relevant. Through various manual searches on databases, you may notice that your research theme has not been invested in high-quality trials and might constitute a good lead for a research avenue!
I wish you good success in your research work!
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Purely asking out of curiosity - we have another protocol that seems successful, so I'm just curious chemically speaking why this might've happened with our first protocol. We initially used a mobile phase of pH 3.0 (MDTM Type II Mobile Phase), and a 2-channel analytical cell set to -100mV and +250mV, where peaks are quantified from the +250mV electrode chromatograph. Despite being the same concentration, HVA peaks are always CONSIDERABLY shorter than all of the other monoamines and metabolites, and consequently detection cuts off at a concentration about 10-fold greater than the other neurotransmitters.
Given the pKa of homovanillic acid (4.4), compared to NE(9.5), DOPAC(3.6), DA(8.93), 5-HIAA(4.22), and 5-HT(9.31), they should all be fully protonated at a pH of 3.0 when suspended in our mobile phase, so I'm not sure why HVA shows such unique differences from the others? Our recording electrode is set to a positive cell potential, so it should be oxidizing (taking electrons from) the sample - could it be that HVA has less 'available' electrons? If so, why is that?
We have supplies coming to switch to a different mobile phase, install a conditioning cell and tackle this problem, but I'm curious to hear why mechanistically this may be happening? Also, again out of curiosity, does anyone know what about a conditioning cell (installed between the column and analytical cell) makes it capable of increasing sensitivity?
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Hi Michael, did this answer your question? Regards, Hendrik
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I am doing research for Parkinson's disease gait analysis. Where can I find a database based on the acceleration of gait from Parkinson's disease patients?
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Patient with neurological problems have different problems. This will impaired their physical, cognitive and even social interaction and so forth.
So, which approach and why that approach is used?
Look into more discussion and information.
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Task-based interventions are highly effective for gait and ambulation among patients with chronic CVA and TBI provided that a sufficient intensity is maintained.
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I am currently working with SY5Y cell line and my goal is to differentiate them into dopaminergic-like neurons for investigations related to Parkinson`s disease. As one of the markers of dopaminergic neurons I have considered using D1 receptor, but I haven`t been able to identify a single study that expressed this type of dopamine receptors in SY5Y cell line by chemical treatment (e.g. retionic acid or TPA) Many did prove expression of D2 and D3 receptors. So I am wondering should I use D1 receptor at all as a marker of dopaminergic neurons?
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Hi Ivan:
People have reported that DRD2 receptor presents in SH-SY5Y cell line, which is upregulated in retinoic acid differentiated SH-SY5Y neuroblastoma. However, for DRD1 receptor, it could probably be expressed also in SH-SY5Y according to the experiment about extracellular dopamine induces the oxidative toxicity of SH-SY5Y Cells by Jian et al. in 2008. However, basically, most of studies use exogenouse expression of DRD1 receptor for the the internalization or characterization of DRD1 receptor in SH-SY5Y cell line, which indicates lower or no expression of DRD1 receptor in SH-SY5Y cell line.
For your reference
Hope this could helps you.
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We would like to roughtly assess the potential neuroprotective ability of a certain agent to prevent people from developing Parkinson's disease (PD). PD has an incidence of 1% in the general population over 60 years. We are planning to conduct a retrospective study on a group of people, who have all been exposed to this agent for many years. The potential beneficial effect of the agent would also consider information about time of exposure to the agent and the estimated total received dosage of the agent during the lifespan. In case if the agent has neuroprotective properties, we predict people who were exposed to it for a longer period at higher dosages have lower overall prevalence of PD than the general population of the same age group. Our concern is - what would be a minimum number of participants who are 60 years old or older, to be able to estimate the agent's potential beneficial effect?
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Hey there,
You need to run a sample size estimation based on your study design. You also need to define/know the alpha (commonly 0.05) and beta (commonly 0.2) levels as well as d. Moreover, if you are planning to run a between-group analysis (case/control as I suppose), you need to know the prevalence of the feature in both your groups separately. I recommend using G*Power (free) or PASS (needs payment) software for a smooth experience. Bests
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If I'm right, dopaminergic neurons in substantia nigra but not in ventral tegmental area are affected by Parkinson's disease. I have stained brain slices with TH to observe changes in dopaminergic neurons in Parkinson's mouse model. In the confocal images obtained after staining, I could not demarcate dopaminergic neurons belonging to the substantia nigra and ventral tegmental area. I'll appreciate it if you could suggest to me the way to find the TH-labeled neurons affected in Parkinson's diseases. I have attached images I obtained and I use ImageJ for TH positive cell counting.
Thank you
Saroj
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Hello,
according to a paper from Thompson et al. in mice (!) you can perform double stainings for TH and Girk2 to determine dopaminergic neurons from the Snpc from VTA (Thompson L, Barraud P et al. (2005) J Neurosci, 25: 6567-6477).
I do not know if this works in rats.
Otherwise you can use the Atlas "Rat brain in sterotaxic coordinates" from Paxinos (or the Mouse Atlas for mice). This can help you to delineate the Snpc from VTA.
Kind regrads
Stefan
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Environmental toxicants induces PD in animal models, one of which is rotenone. Controversies exist on whether the stereotaxic technique or systemic administration is the best. While some have argued that there is high mortality using the systemic method compared to the stereotaxic surgery method. Which method best replicate the pathological hallmarks of PD?
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Thanks
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I'm a retired research chemist/physicist with Parkinson's disease and I've been working on upregulating Nrf2 with sulforaphane to fight oxidative stress.
The results I achieved on my PD and with a group of 8 people with PD have shown that sulforaphane strongly attenuated non-motor symptoms especially fatigue and lack of motivation, suggesting that the first target for Nrf2 seems to be mitochondria. I am not an expert in this subject and I would like to reach out to research groups and Parkinson's disease specialists to discuss how to take this idea further.
You can find the background here :
And a preprint I have written on RG here:
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I have been using 400 micrograms twice a day. Brand: Swanson.
I have had the drug checked at the University and they confirmed it is 87% pure sulforaphane. Not the 99% the lab says. But is good enough for me.
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Hi,
I'm working on poison induced Parkinson in rats and I do apply some behavioral tests to check Neuropathic pain.
As a result, I find out that they simply show signs of neuropathic pain ( increased mechanical allodynia meaningfully) exactly on the same side I applied lesion to VTA, Substantia nigra and striatum through stereotaxic surgery.
Knowing that there is decussation (crossings in the form of an X, relate each side of the brain to the opposite side of the body.) As a physiological normal situation.
Does anyone have the same experience?
Or Does anyone can explain this complicated result?
I assure you that I have done surgeries and behavioral tests with certitude.
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Martha Isabel Dávila-García Thank you dear Martha, very well explained. Firstly, I thought SNpc unilateral lesions will cause nonmotor symptoms such as pain on contralateral side of the body. So I performed experiments 3 times and I obtained the same results each and every time. Also I found out with disease progression neuropathic pain was observed on the both sides.
Again thanks for your answer. I appreciate it.
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I am trying to assess spatial memory in MPTP induced Parkinson's disease C57Bl6 mice using a Morris water maze. I wanted to know if there are any specific dimensions to the MWM to be used. Most papers suggest using 120 cm diameter with 40 cm height . Has anyone used a maze smaller in diameter than this?
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@ Ghulam Md Ashraf - thank you for your response.
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I have tried administering rotenone intraperitoneally to C57Bl/6 mice in my lab, but there is high mortality rate. Subcutaneous rotenone at a dose of 2.5 mg/kg for 28 days did not show any changes in alpha synuclein levels. I m in need of an acute rotenone model of PD, in which I can check the effect of molecule against alpha synuclein aggregation.
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choosing sc. injection was a good decision. However, 28 days is not enough. extend the days to 40-50 days and you will probably see the Lewy bodies. You can visit my latest article in this regard:
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I have some files about PET-DAT in patients, having parkinson disease. And I use spm12 implemented in matlab15b for coregistration and spatial normalization of images and voxel-based comparison. But I do not know how to measure regional uptake values for region of interests, like putamen, caudate.
Can you offer some methods and Suggestions?Thank you very much for your help.
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You nees ROIs of the regions.
Marsbar will do the trick
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Hello Research Gate community,
we are currently trying to differentiate SH-SY5Y cells into dopaminergic neurons. However, every protocol we tried so far did not work out. We tried to induce directed differentiation using RA for 5 days following supplementation with TPA for 5 days in various concentrations (as recommended in several papers). We tried differentiating using RA for 5 days followed by 5 days of BDNF treatment, which also did not work out. Are there more things we have to keep in mind as for example low glucose media or supplementation with Glutamine? We usually use standard DMEM with FCS and Pen/Strep. We would be very happy for any advice.
Thanks a lot for your suggestions.
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Firstly, you need to plate your cells as per your experiments, be careful about the density of the cells you need to differentiate. If you plate much cells they won't grow neurites or processes and they will die if you plate too less!! You should plate cells so that they can communicate! Secondly, for your ref, plate 100,000 cells in one well of 6 well dish in complete medium with 10%FBS!! Next day, add RA in Medium with less serum (1-5%) and it works really well. Change the medium every alternate day and be careful about RA, because retinoic acid is very sensitive to light exposure and after 5 days add BDNF along with RA in medium with no serum!! Thirdly, we didn’t see TH levels, but other papers have shown good images of TH in Blots and Icc
hope it works for you
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Current genomics tools to to discover new or study current biomarkers of neurodegenerative diseases.
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Do you know what is metagenomics? And did you read the question well?
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Hi Jung-Min Lee, sorry to bother you, but we are developing a project to study Physical Activity in Parkinson Disease patients, but we can not download the specific software to work with the sensors. So, can you ask the person who worked for the Sensewear Armband how is it possible to download the software needed to work with the system (sensors)?
If you intend to put me in contact with that person my email is
Thank you.
Best regards, Filipe Melo.
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Filipe M. S. Melo There is a typo on the website, try intalling the 7.0 file which actually contains v8.1 named sensewear-8.1.0.22-20140915.exe
Nara da Silva Dias I see that the main issue is that the hyperlink to install MS visual 2008 is no longer a valid url. I found a workaround and got it to work eventually by following these steps:
1. Go to https://www.microsoft.com/en-gb/download/details.aspx?id=29 and install the "vcredist_x86.exe file by clicking the download button and selecting that file.
2. Install vcredist_x86.exe which is the visual package required for Sensewear.
3. Go to "sensewear-8.1.0.22-20140915.exe", right-click and go to properties > compatability tab and change the compatability mode to Windows XP(Service pack 3), click apply.
4. Try running the installation file again.
Please let me know this works for you and please recommend this answer so that others can see it.
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Patient diagnosed with intractable major depression. Olanzapine treatment caused severe drug-induced Parkinsonian symptoms. Olanzapine discontinued 18 months ago and patient recovered from DIP. What alternative medication would you recommend?
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one could take advantage from tricyclic antidepressant: used cautiously, these old but still valuable drugs might be especially useful in case of Parkinson(ism)
regards, MC
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We investigate the mechanisms of Parkinson's disease and do drug design for Parkinson's disease. We use theoretical physical chemistry, biophysics and bioinformatics in our studies. We are in need of experimental collaborators to apply for funding from the Michael J Fox foundationand COST EU projects. Are you interested? 
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Good answer dear Orkid Coskuner
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One of the current Models prepared to cure Parkinson's disease is based on the process to derive Brain cells from Skin Cells. Is the same possible?
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Following.
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Does anyone have a tip/hint on how to deliver physical assessment remotely? References are welcome! I am working on a project to deliver physical exercises remotely to older people and people with Parkinson's disease, however the research team would like to assess participants' progress too. #COVIDー19
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Hello Paulo Henrique Silva Pelicioni,
Comfortable gait speed is a non-invasive indicator of physical condition. Aging or illness reduces the energy capacity of the body. Part of this power is spent on movement. It is equal to the force spent on movement (F) multiplied by the speed of movement (V), i.e. FV. F is roughly the same (we consider the body weight the same). Then an increase in the comfortable gait speed will indicate an improvement in physical condition, and a decrease in the gait speed will indicate its deterioration.
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Sleep problems can be seen in patients with Parkinson's disease. Can it be about serotonin?
In mice, ablation of the raphe and no production serotonin increases wakefulness and impairs the homeostatic response to sleep deprivation.(DOI:https://doi.org/10.1016/j.neuron.2019.05.038)
Even in the absence of depression, the CSF levels of 5-I-HAA of patients with Parkinson’s disease are lower than those of age-matched controls.
( DOI: 10.1176/jnp.2.1.88 )
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Thank you for great articles. They gave me a new perspective about PD.
I want to suggest an article: Serotonergic dysregulation is linked to sleep problems in Parkinson's disease (doi:10.1016/j.nicl.2018.03.001)
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since apomorphine is not availble, and pramipexole and apomorphine are both dopamine receptor agonists, so I'm wondering if I can use other dopamine receptor agonists to verify the rotation test of 6-OHDA induced PD mouse model.
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/LABORATORY ANIMALS: Acute Exposure/ A 0.1% injectable solution of pramipexole injected paravenously into the jugular vein was conditionally tolerated by rats. Single intravenous injections of pramipexole 0.1% solution into the marginal vein of the ear were tolerated by rabbits. Single intraarterial injections of pramipexole into the central artery of the ear were tolerated by rabbits. Health Canada; Product Monograph for Mirapex (Pramipexole Dihydrochloride) Tablets, Drug Identification Number (DIN): 02237145 p.41 (Date of Revision: November 27, 2012). Available from, as of June 12, 2015: http://webprod5.hc-sc.gc.ca/dpd-bdpp/start-debuter.do?lang=eng
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Why is running in Parkinson's disease both possible and have therapeutic effects in contradistinction to walking?
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I think that the attached video link might yield some interesting insights that could be parlayed into controlled investigations if anyone is interested.
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Hi Everyone. I am trying to check the neuroprotective activity of some compounds in the rotenone model of Parkinson's disease in PC-12, for which I will check the effect of that compound on cell viability first. I want to ask whether it is required to differentiate PC-12 for this purpose, as I tried to differentiate the cells using 30 ng/mL as well as 50 ng/mL NGF. I am able to see the differentiated cells in 3-4 days in 96 well plate, but NGF itself is causing cell death, which could be a variable for the cell viability test.
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Hii Suriaya. I am currently seeding 5000 cells per well in 96 well plate. I will try with 2000 cells per well for this time. Moreover, I am also getting cell death in 6 well plate, where I am seeding 5,00,000 cells per well. Please suggest if I can differentiate using less dose of NGF.
Thank you
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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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We are seeking to identify the major barriers Parkinson's disease patients face in obtaining care for mental health issues. What are the major gaps in treating mental health disturbances in this population?
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We had a mouse model of PD and check if exercise in a running wheel decreased the damaged neurons or stopped the degeneration of them. If you are interested I attach the paper:
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Hello,
I'm currently designing a protocol in Parkinson's disease and I was wondering about the optimal timing to test motor symptoms in relation to last dose of dopamine agonist(s).
It is clear to me that standardisation of this aspect is essential, but I could not find specific literature with recommendations in this regard.
Any pointers to papers or opinions on this matter would be immensely appreciated.
Thank you
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Thanks for your response Victor, it is very helpful and the reference to the LED is also much appreciated!
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I want to test the effect of a neuroprotective drug on rotenone rat model of Parkinson's disease but after reading the related articles about my work, I became doubts about select the best dosage of the drug and treatment methods. in some of the articles they using a low dosage of a neuroprotective drug and in some high dosage and their treatment was different in some cases, they use the oral method and some intraperitoneal injection method.
Does anyone have any suggestions to select the best dosage and treatment (o.p or i.p)?
Many thanks
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Do you know the highest dose that does not produce an adverse effect? If so, this is your NOAEL. A dose 10 fold lower than this should be you maximum dose to ensure a good margin of safety. You will then need to use this a start point for dose response analysis. Starting with the NOAEL dose you need to back down by ten fold increments to the next two lower doses. For example, if the NOAEL is 100 mg/ kg your dose response analysis should start with 1mg/kg, then 10 mg/kg then 100mg/kg. This should give you a good baseline set of data that can be translated to NHP and humans using allosteric modeling.
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Can histone deacetylase activity influence the progression of Parkinson disease? If so, what are the underlying mechanisms?
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You might be interested in our PD models:
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Current researches to cure Parkinson's disease deal with the formation of the dopaminergic neurons from the Skin fibroblasts but even after the formation of neurons, is their administration to the Hippocampus region of Brain possible?
If yes, is that economically feasible?
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Great study discussion with senior neurosciences Professor anatomy and physiology will guide you better to understand brain and spinal cord,
Skin is also very important, understand your question,
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Parkinson's Disease is a seerious issue now days.
Yoga may be a way of manage this problem. What yoga practice should be provided to them?
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The results of recent review found that practicing yoga helped improve functional mobility, balance, and lower-limb strength in people with Parkinson's disease. In addition to improved balance, flexibility, and posture, participants experienced a boost in mood and better sleep quality.
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I have found only a handful of studies in my review of literature. Just wondering if anyone is looking at this also.
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Please take a look at this useful RG link.
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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!
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I'm looking for the biochemical explanation behind the creation of genetically modified organisms (GMOs) for use in research of human pathologies such as Parkinson's Disease (PD) or Huntington's Disease (HD). I will really appreciate any answer or recommendation of literature.
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Remember that animals have four paws/legs on the ground but humans only two. Therefore magnetic fields from remanent magnetism or magnetism in the lab however caused will vary in bodily absorption between man and animal. EMF levels in labs can be very high - are the labs shielded ? Reactive Oxygen Species from unpaired electrons are of very high significance in adverse effects.
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I'm interested to continue with brain signal research in case parkinson disease. I'm searching for EEG data for the same or interested to work with the research groups in the same field.
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The data which I have it not on EEG - it is on gait monitoring. Sorry. If you would like I can forward its link.
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Hi, we're working on a pilot research and our aim is to develope parkinson dis. with both intranuclear and intraperitoneal injection methods.
In i.p. model The problem is rats can not tolerate the protocol recommended in articles [ examined dosages : 2-2.5 mg/kg dissolved in DMSO and diluted in MCT i.p. injection ]. We found Rats dead after 2-3 consecutive days.
What's the solution ?
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I definitely agree with trying relatively lower doses and spacing out injections like what was suggested. If this does not lower to an acceptable mortality rate, you may try another compound,
MPTP (1-methyl-4-phenyl-1,2,3,6-tetrahydropyridine), that works similarly to rotenone.
Have you had any autopsy done on the animals to determine the cause of mortality? It may be revealing to see if there was a direct toxic effect on intraperitoneal tissues.
Good luck!
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Need to consider all variability arising from age, gender, post mortem interval etc.
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use SPSS latest version & you will find sample size after feeding basics of your requirement into software. Than ask for sample size it will display sample size.
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Here is the latest example of our 20 years of cognitive dissonance. That the "heterogeneity of PD" remains "a major problem" but that better techniques (such as "utilization of complex analysis strategies and automated standardized assessment methods") will circumvent it. If even LRRK2-PD, as indirectly suggested by the authors, represents a collection of different diseases, can we rely on the brute force of newer and sophisticated analytic methods to bring us out of the conundrum that our unabated allegiance to PD as a unitary disease construct brings? Our field remains stuck in the quest to validate the century-old clinico-pathologic, convergent model of disease nosology, unlike most other fields of medicine, ahead by three decades of embracing systems biology divergence. No analytic technique will overcome the basic flaw in our ongoing biomarker-discovery efforts: that we, clinicians, get to set the gold standard against which to validate biology. It should be the other way around: biology validating disease subtypes. Unless we start walking the talk of PD as a syndrome of many biologically distinct diseases --we will continue banging our heads against the same wall. It is time to move beyond the search for biomarkers of convergence. Whatever is found to be common to all forms of PD is unlikely to be pathogenic in any.
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Thank you for taking the charge against this matter. I share your concerns and opine them to any willing listeners.
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I wanted to work on developing a deep Learning model to differentiate different classes of disease and controls. But I am not able to find the required database for it. Can someone suggest me where I can find one?
Or can anyone tell me how do I look for database related to particular icd_9 codes?
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We already know the application of botilinum toxine drooling in patients with Parkinson's disease. We often recommend that you swallow saliva and chew gum. What are the methods you use in your daily practice?
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You may want to consider Glycopyrrolate (Glycopyrronium bromide) as a anti-cholinergic drug. See also:
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Parkinson's disease (PD) is a neurodegenerative disorder that affects predominately dopaminergic neurons in a specific area of the brain called substantia nigra. While Parkinson’s itself is not fatal, disease complications can be serious. The Centers for Disease Control and Prevention (CDC) rated complications from PD as the 14th cause of death in the United States.
Currently, all therapies used for PD improve symptoms without slowing or halting the disease progression.
So at present what is the life expectancy of a Parkinson's patient?
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This is a very and unique occasion to partecipate at the first convention in which patients, caregivers and Doctors will work toghether in a brain storming....
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Dear Stephania,
The convention has already passed but we developed a PD model (mice) and tested the beneficial effects of physical exercise. It may interest you:
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Hi,
I've been doing several western blot trying to check protein expression, oligomer formation and protein degradation in alpha synuclein in cell lines (SH, PC12 and HEK) after transfection with plasmids (pIres).
I've had a lot of varibiality in my results and I don't know what I'm doing wrong, or why I have such variability in my blots that make them non consistent.
I don't use native gels, but I still see monomers, dimers, trimers and tetramers of alpha synuclein.
I've tested Old and fresh RIPA buffer. I've also tested membrane fixation with 0.4% PFA which improve a bit the bands.
Sometimes I get monomers and dimers for SH, and dimers, trimers, and tetramers for PC12, and sometimes only monomers in SH, and only tetramers for PC12.
I've get other weird results like no tubulin in PC12, or only GFP in the lane where is the C- with pIres emtpy vector only expressing GFP, but not in the rest of lanes with pIres expressing alpha synuclein and GFP (and I confirm that cells were green).
So, I'm desperate and I will appreciate all your help, please!
Attached the procedure and also some images.
Thanks!
The detailed protocol is:
Cells in 24 well plate as C- or transfected with pIres plasmid with alpha synuclein-6xHis tag and GFP
- Remove medium
- Trypsinize and inactivate. Collect in a eppendorf and add 500 ul of PBS to wash them
- Centrifuge 5 min 300 g RT
- Aspirate the SN and freeze the pellet in dry ice. Store the samples at -80ºC
- Lysis buffer: RIPA (50 mM Tris-HCl pH 7,5; 1% TritonX100; 1% NaDeoxycholate; 150 mM NaCl; 1 mM EDTA; 10 mM NaF) + 100x Halt Inhibitor
- Add 100 ul per sample of lysis buffer and vortex until pellet get resuspended. Incubate 30 min on ice and vortex at minute 15.
- Centrifuge 10 min at 4ºC 10.000 rpm
- Transfer the supernatant to a new epp and store the SN and the pellet at -80ºC until use.
- BCA quantification using 10 ul of sample
Western blot:
- 5-10 ug of sample + 4x loading buffer (10% b-mercaptoethanol), 95ºC 10 min + spin
- Load the samples on Precast Gel TGX Biorad (4-20%) Electrophoresis: 100 v 1h 30 min
- Open the cassete in transfer buffer and place the gel over the PVDF membrane (BIORAD already prepare for Tran Blot Turbo System (semy dry system). I usually soak the transfer cuvette, filters and membrane and remove the excess of buffer. Transfer of a mini (2.5A cte up to 25 V 3 min) or a midi or 2 gels (2.5 A cte up to 25, 7 min) gel to PVDF membrane
- 1x TBS wash
- 0,4% PFA fixation 30 min RT
- 2x TBS wash
- Ponceau staining 5 min
- 3x TBS-T wash
- Blocking 5% milk in TBS-T (1-2 h RT)
- Primary antibody rabbit anti alpha synuclein (PA5-17820) 1:1000 in TBS-T ON at 4ºC
- 3x TBS-T wash
- Secondary antibody goat anti rabbit –HRP 1:40.000 1-2 h RT
- 3x TBS-T wash
- Dry excess and put in a dry tray
- Develop with SuperSignal West Pico PLUS Chemilluminiscence (2 ml of mixed buffers and incubate 5 min).
- Remove the excess of substrate and place it between transparent plastic
- Imaging with Amersham 600RGB (1sec, 1 min and incremental ever 1 or 3 or 5 min....)
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Hi Ana, I'm having some difficulty following your experiment, a bit too many uncertain points... then of course giving you any suggestion is difficult. So let me do some troubleshooting and ask you a few questions: 1) How is your plasmid engineered? Who is controlled by the IRES, the GFP (I hope so) or the alpha-synuclein? (This could explain why you lose expression of the GFP in the full vector, if the Cap-dependent translation is working well, the IRES-dependent translation will be less efficient. But if there is no CDS before the IRES, there is no competition on the mRNA and the IRES-dependent translation will work better. IF is more sensitive than WB, for this reason you probably detect some fluorescence at the microscope. Moreover a smaller plasmid might also be better transfected into cells, so more copies could enter a cell or more cells be transfected. Lastly, they are two different plasmid preps and one might have come out cleaner, one less, affecting differently the transfection efficiency - seems the case of the GFPblot image, top blot, see point 2) 2) Which cells are expressing endogenous alpha-synuclein? I can see that SH cells do (you see the doublet at 20 kDa, the top band being your His-tagged version, in the Nooligomers picture, top blot). This means that in the top blot of the GFPblot image you did not transfect the cells, or the transfection efficiency was too low (few cells, or too little plasmid per cell), and the His-tagged band is missing from the WB. Anyway the GFP band in the C- is already pretty weak...). PC12 cells also express alpha-synuclein, but it's rare to see your His-tagged version and the endogenous in these cells, anyway in the bottom gel of the GFPblot image something went wrong with the WB or the PC12 extracts, all signals are too low, and when a-synuclein monomers are so weak you can't expect to detect GFP expressed from an IRES. Finally HEK cells... impressive, they seem to express low levels of a-synuclein, all your C- controls show a weak band at the right height. Anyway, it's a good control to verify that you are transfecting your cells. Secondly, they never show tetramers... Possibly the formation of the multimers is concentration-dependent... 3) The multimers: What you see at 75 kDa, ONLY in PC12, I personally doubt it's tetramers, it seems a non-specific band from the Ab recognizing something in PC12 (in the Notubulinin PC12 image you have this band in the C- where you don't even detect the tranfected monomer nor the endogenous...). Anyway, if you have sure evidence that it's tetramers, keep in mind you see them only in PC12. You are boiling the protein extract in SDS and you are running a denaturing gel... it's difficult to imagine aggregation of such a small disordered peptide... Also what you call dimers, which you detect at the same level in transfected and C- samples or with stochastic intensity levels.... very suspicious... Have you ever checked your Ab on a a-Syn KO or KD extract? I would do it... or test a different Ab... So, you are right, it looks quite chaotic. You also seem to have protein degradation, at least sometimes (the 25 kDa tubulin band in the bottom blot in the Nooligomers figure). To start, you can try to improve a few things in the protocol: 1) My suggestion is to lyse the cells directly on the plate on ice: remove medium, wash twice with warm PBS like if you should passage the cells, remove thoroughly the PBS and place the plate on ice. Then add the 100 ul of ice-cold lysis buffer on the cells in the well. Pipette to help the lysis a few times in the well and transfer in tube. Do not vortex, there is no need, the RIPA is strong enough (in fact the TritonX would also suffice) to lyse. You can shake the tube once in a while with your fingers or pipette while you incubate on ice. Incubate 15 min on ice. Never bring native protein extracts at room temp, always on ice. 2) Proteins are delicate! Thawing and freezing degrades them quickly, denatures them and induces aggregation depending on the protein type. My suggestion would be if you only need them for WB, immediately after lysis quantify while keeping the lysate on ice and then denature them with Laemmli and boil. Denatured proteins dstill degrade when thawing and freezing, but more uniformly and less. Store in 50 ug aliquots at -20 (so that you thaw and freeze the only 5 times). Anyway, if you wish to freeze them native, then you should shock-freeze them in liquid nitrogen. 3) WB. I had quite bad experience with semi-dry blotting. It is very uneven... and I believe you are experiencing this quite clearly. My suggestion would be to try a few blots with the submerged method. It's longer (70 min at 110 V), it uses more buffer... But you will be surprised by the result... Then don't forget what I mentioned above... test a different Ab or try to obtain or produce a-Syn knock-out or knock-down protein extracts... Good luck.
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Why taste sensation is altered by levadopa?
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Taste and smell are related. there is a good literature on the loss of smell in PD.
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I am started studying on Parkinson's disease, which is neurological disorder...is their any characterization should i follow to study and their prevention.
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Vedad Delic thanks for your answer
we are looking for another human cell line that might like SHSY-5Y, with the ability to differentiate to serotonergic/ gaba like neurons
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Hi
Plz suggest from where i can get mri brain image dataset for parkinson disease.
Although i have applied from ppmi, but it will take time.
Thanx
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does anyone know a questionnaire that can be used for a research to assess impulsive‐compulsive disorders in Parkinson's disease
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Ah sorry !
you research it ?
I had assessed impulsive disorders in huntington disease but I am not sure that it could be used for parkinson’s disease ?
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Has anyone tested residual pesticide levels on Fruit and Vegetables? Before and after washing? Does washing fruit remove enough of the residual pesticide?
What is the cumulative pesticide dose over decades and does it play a role in diseases like Parkinson's Disease?
Are pesticide manufacturers culpable for any long term side effects?
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Pesticides are a group of chemical compounds that can have different negative effects on health. The EFSA annually publishes the EU report (European Union report on pesticide residues in food) on pesticide residues and health risk assessment: https://www.efsa.europa.eu/en/press/news/170411
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Hello,
I'm trying to induce PD in mice (NOD-SCID) but when apomorphine is given, they do not spin. Do you know some tricks how to do it (maybe a protocol) how to store 6OHDA (I have one from Sigma with ascorbic acid, I have solved it, I have made aliquots and I have kept it in -20) and how to administrate apomorphine (how to store it?). I don't know where is the problem.
best,
Anna
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Hi Anna,
I would like to add one more thing. There should be significant loss of dopamine in the striatum of the 6-OHDA injected site, so that proper contralateral rotation can be seen following subcutaneous apomorphine treatment. Sometimes, if the ear bars of the mice are not properly fixed in the stereotaxy apparatus, and the coordinate of MFB is altered, then the injected toxin might reach some other part of the brain, and consequently expected dopamine depletion can't be found. Secondly, like apomorphine, 6-OHDA should also be made fresh and dissolved in anti-oxidant solution like .01% ascorbic acid, otherwise 6-OHDA will be readily oxidized.
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I'm searching an available dataset of accelerometric or EMG tremor recordings in Parkinson's disease patients and/or essential tremor patients. Is there anyone that knows some available online datasets, or has this kind of data and is interessed in a collaboration for a study? I already have 4 different datasets of tremor recordings.
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I acquired data of 52 PD patients, for this paper:
If you are interested please send me an email:
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Much research has been done on the effects of specific genetic variants on the symptoms, age of onset, and progression of the disease in familial Parkinson's. Not much is available to date on the interplay of polymorphism of multiple pathogenic variants, specifically the major variants being studied for possible treatment and cure - LRRK2 G2019s and one or more of the many SNCA variants. As this IS occurring in multiple Parkinson's patients, what findings are there in the disease presentation and patient experience?
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Hi Reni, very interesting question and one we do not have the answer to at the moment. Human studies are ongoing, and recent BAC transgenic rats and mice were employed to help answer these questions. While G2019S-LRRK2 mutation is the most common genetic cause of late onset PD, it is not found in patients that also have the mutation in the SNCA. SNCA mutations typically cause early onset and very aggressive PD. However, when G2019S-LRRK2 mutants (primary neurons or mice) are exposed to fibrilized alpha synuclein, they fair much worse than WT according to work done by West, and Volpicelli, but this work is ongoing and some models do not show drastic susceptibility (Virginia Lees lab for example). I personally think the relation between LRRK2 and SNCA is indirect, and may occur through Rab family proteins, recently found to be bonafide biological LRRK2 substrates. While I could not give you an exact answer I hope the info is useful and please reach out should you have any additional questions, if I cannot answer them specifically I can probably direct you to someone who can (and they might not be on researchgate).
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The disease is the same as tremor at rest, the more prevalent it is in aging, but it is also found in young people. The prevalence is the same in all regions of the world, ie the percentage of the outbreak does not vary much with the change in the region. In general, the disease occurs due to the loss of the secreting cells of a substance called dopamine (a neurotransmitter). Increasing the ratio of acetylcholine to dopamine in the cerebellum glands causes tremor symptoms, muscle stiffness and slowness of movement.
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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.
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I am trying to find a practical way to organise the information that I have about the medication that my participants have been and are currently taking. Our study is looking at the effects that a weekly community-based exercise class has on Parkinson's disease. Every 10-12 weeks we assess our participants (different health, functional, cognitive tests and plasma/saliva samples). In order to control for the effect that medication can have, I ask our participants to report the different drugs that they are currently taking and any medication changes. However, I am finding it quite difficult to organise this data in an efficient way in excel or to track for changes and analyse it.
Is there anyone with experience in running similar longitudinal intervention trials that could suggest me a way to do it?
Many thanks
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Sorry for my late reply. Thank you so much for the article that you have shared with me. It is definitely very useful.
Best wishes,
Anna
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I found multiple publications referencing this dataset but have been unable to find a link to request access to the data.
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The study is registered in ClinicalTrials.gov
You may try to get in touch with the contacts reported
Contact: James Beck, PhD 1-800-473-4636 jbeck@parkinson.orgContact: Fernando Cubillos, MD 1-800-473-4636 fcubillos@parkinson.org
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Whether the changes in the cytoplasm and nucleus are symmetrical or they differ ? Whether the morphological changes are dose dependent ? or species dependent ?  
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Background Information: A good dance friend of mine recently revealed to me that he has Parkinson's. During a recent dance clinic I decided to use what I know about music and Parkinson's (music helps improve movement) in order to see how it impacted his symptoms over the course of the week. At the beginning of the week, his symptoms were rather mild and music, when paired with dance, made him appear as if he was never diagnosed with Parkinson's. (Sometimes, even hours after listening to music or dancing, one would not be able to tell!) As the week went on, despite the music that was playing or the opportunities to dance, his symptoms appeared to worsen. To what extent does music help these individuals? What does exhaustion do to the brain that no longer allows music to help with motor functioning? What do I seem to be missing when reading this research? Many thanks!
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