Means a lot to me. Thank you respected sir for such an informative video it really helps me a lot in clearing my confusion and in my assignment making.
well, as per my knowledge you have missed the work of secretases as Alpha and Gamma secretases cause a healthy breakdown of protein while beta cleavage is misdirected. But in the video, you said gamma-secretase cleavage cause disturbance that's not true. Please go through the latest articles and correct me if I am wrong. Thanks
Hi, very good work, thank you. I have a question : what is the link between Tau misfloding and hyperphosphorylation of Tau ? Does Tau is hyperphosphorylated because it is misfloding ? If someone anserw to my question, I thank him in advance. Happy new year 2022!
No problem: 1) molecular characteristics of alzheimer's disease: science.sciencemag.org/content/358/6359/45/tab-figures-data 2) Tau microtubules: www.sciencedirect.com/science/article/pii/S0531556516305800 Other picture: 3) molecularneurodegeneration.biomedcentral.com/articles/10.1186/1750-1326-2-22
this is honestly not right at all in regards to pathophysiology and microphysiology of how plaques and tangles are caused . The basics are mentioned just not the intricacies on how everything comes together. for example tau proteins don't unfold , they’re hyper polarized through hyperphosphorylation from the amyloid beta plaques outside the neurons themselves causing clumps giving a weak cytoskeleton within the neuron. Then with the weak and half dead neurons they clump up and cause neurofibrillary tangles. Amyloid beta plaques are a whole other beast, they’re outside the neuron not within the neuron.
Had exactly this doubt, I'm learning about prions and the diseases they cause. I think the PrP protein has nothing to do with tau and amyloid beta right?
@@celinat8622 Other resources say it is double prion disease involving tau prions and amyloid prions, which is difficult to believe. I believe the researcher is Prusiner.
The intro killed me😂
It's stupid
@@israelduarte1189 and that's why it's (somehow) funny
Very well explained both pathways, thank you
Means a lot to me. Thank you respected sir for such an informative video it really helps me a lot in clearing my confusion and in my assignment making.
Fantastic summary, thank you
well, as per my knowledge you have missed the work of secretases as Alpha and Gamma secretases cause a healthy breakdown of protein while beta cleavage is misdirected. But in the video, you said gamma-secretase cleavage cause disturbance that's not true. Please go through the latest articles and correct me if I am wrong. Thanks
Muy buen video ! Thank you so much ...greetings from Perú :)
Thank you, Aurora!
Hi, very good work, thank you.
I have a question : what is the link between Tau misfloding and hyperphosphorylation of Tau ? Does Tau is hyperphosphorylated because it is misfloding ?
If someone anserw to my question, I thank him in advance.
Happy new year 2022!
Hey Kevin, could you post a link to the articles that you used for this video, i would like to credit the pictures :)
No problem:
1) molecular characteristics of alzheimer's disease: science.sciencemag.org/content/358/6359/45/tab-figures-data
2) Tau microtubules: www.sciencedirect.com/science/article/pii/S0531556516305800
Other picture:
3) molecularneurodegeneration.biomedcentral.com/articles/10.1186/1750-1326-2-22
Thanks man, but I have a question what is sAPP
merci beaucoup !
50% of patients with the plaques do not exhibit Alzheimers symptoms so I would rule that cause out. How does a prion develop? That is the question.
I was wondering, why does the calcium influx cause apoptosis and not necrosis?
Because the Ca+ itself is considered an apoptosis signaller at a certain level, I think. pmc.ncbi.nlm.nih.gov/articles/PMC1569591/
So helpful
Thank you soooo much
the intro made me question everything
Thanks for the informative video, the intro is a bit fucked but everything else is gold. Cheers Cobba
Is ALS a Prion Disease?
this is honestly not right at all in regards to pathophysiology and microphysiology of how plaques and tangles are caused . The basics are mentioned just not the intricacies on how everything comes together. for example tau proteins don't unfold , they’re hyper polarized through hyperphosphorylation from the amyloid beta plaques outside the neurons themselves causing clumps giving a weak cytoskeleton within the neuron. Then with the weak and half dead neurons they clump up and cause neurofibrillary tangles. Amyloid beta plaques are a whole other beast, they’re outside the neuron not within the neuron.
Had exactly this doubt, I'm learning about prions and the diseases they cause. I think the PrP protein has nothing to do with tau and amyloid beta right?
@@celinat8622 Other resources say it is double prion disease involving tau prions and amyloid prions, which is difficult to believe. I believe the researcher is Prusiner.
Filamin A