4 ms·

Not to unnecessarily shit on the parade, but I’m not sure this is by itself all that exciting, and calling it a breakthrough seems like an exaggeration. Diagnos

by avazhi 3y ago

Not to unnecessarily shit on the parade, but I’m not sure this is by itself all that exciting, and calling it a breakthrough seems like an exaggeration. Diagnosing Parkinson’s isn’t really an issue - worst case you give the putative sufferer Levadopa and see if they respond. If they do, they’ve got Parkinson’s. Not sure how much this really changes the time horizon for an actual treatment. It’s progress, ostensibly, but I’d quibble with categorising it as a breakthrough.

fatfingerd 3y ago
Finding subtypes before clear symptoms is obviously superior for testing earlier intervention and allowing patients to make a living will with fuller faculties.
echelon 3y ago
> I’m not sure this is by itself all that exciting This actually seems pretty significant. 1) It gets us closer to understanding the pathology: >> It also suggests that alpha-synuclein aggregation in spinal fluid is not a life-long trait but rather acquired as part of a disease biology process that ultimately gives rise to symptoms. 2) It gives us a higher resolution of detection. >> αSyn-SAA can distinguish Parkinson’s from control volunteers with a stunningly robust sensitivity of 88 percent and specificity of 96 percent. 3) It shows different disease subtypes or mechanisms: >> These results suggest that not all cases of clinical Parkinson’s symptoms are associated with the accumulation of alpha-synuclein aggregates as detected by this assay, and that LRRK2 variant carriers, in particular, may not show this pathology. 4) It gets us earlier signal: >> This finding suggests that synuclein pathology could be detectable by this assay earlier than dopamine dysfunction is seen with DAT imaging, extending the window in which it may be possible to intervene with preventive therapies. This is a valuable tool that will shed light on the entire disease pathology and guide further research and investigation into treatments.
threeseed 3y ago
They are working towards not requiring spinal fluid for the test. So it's possible that it could end up being a non-invasive test that could be done at regular intervals early in life. Especially given that 15% of people with Parkinson's have a family history.
PaulKeeble 3y ago
Biomarkers are extremely important in any disease. They make diagnosis very clear cut but that isn't the main reason they are necessary. What a biomarker really does is focus research for treatments, you know precisely what it is you have to change and to what level and how to measure it. This makes it a easy to target drug development and to measure whether it works. Without a biomarker you never know if the drug being developed will help or not and most drug companies stay away from diseases without one.
- FollowingTheDao 3y ago
  The problem the OP pointed out is a valid one. Alpha-synuclein is a biomarker for many neurological diseases https://pubmed.ncbi.nlm.nih.gov/24262191/ https://pubmed.ncbi.nlm.nih.gov/24262191/ So you might say someone has a marker for Parkinson's and they might get another neurological disorder. They tried these treatments in Alzheimer's and it failed. Why? because it is just another symptom and not the fundamental cause of the disease. It is a good biomarker for poor health, but it is not a good biomarker for any specific disorder.

by avazhi 3y ago

fatfingerd 3y ago

Finding subtypes before clear symptoms is obviously superior for testing earlier intervention and allowing patients to make a living will with fuller faculties.

echelon 3y ago

> I’m not sure this is by itself all that exciting This actually seems pretty significant. 1) It gets us closer to understanding the pathology: >> It also suggests that alpha-synuclein aggregation in spinal fluid is not a life-long trait but rather acquired as part of a disease biology process that ultimately gives rise to symptoms. 2) It gives us a higher resolution of detection. >> αSyn-SAA can distinguish Parkinson’s from control volunteers with a stunningly robust sensitivity of 88 percent and specificity of 96 percent. 3) It shows different disease subtypes or mechanisms: >> These results suggest that not all cases of clinical Parkinson’s symptoms are associated with the accumulation of alpha-synuclein aggregates as detected by this assay, and that LRRK2 variant carriers, in particular, may not show this pathology. 4) It gets us earlier signal: >> This finding suggests that synuclein pathology could be detectable by this assay earlier than dopamine dysfunction is seen with DAT imaging, extending the window in which it may be possible to intervene with preventive therapies. This is a valuable tool that will shed light on the entire disease pathology and guide further research and investigation into treatments.

threeseed 3y ago

They are working towards not requiring spinal fluid for the test. So it's possible that it could end up being a non-invasive test that could be done at regular intervals early in life. Especially given that 15% of people with Parkinson's have a family history.

PaulKeeble 3y ago

Biomarkers are extremely important in any disease. They make diagnosis very clear cut but that isn't the main reason they are necessary. What a biomarker really does is focus research for treatments, you know precisely what it is you have to change and to what level and how to measure it. This makes it a easy to target drug development and to measure whether it works. Without a biomarker you never know if the drug being developed will help or not and most drug companies stay away from diseases without one.

FollowingTheDao 3y ago
The problem the OP pointed out is a valid one. Alpha-synuclein is a biomarker for many neurological diseases https://pubmed.ncbi.nlm.nih.gov/24262191/ https://pubmed.ncbi.nlm.nih.gov/24262191/ So you might say someone has a marker for Parkinson's and they might get another neurological disorder. They tried these treatments in Alzheimer's and it failed. Why? because it is just another symptom and not the fundamental cause of the disease. It is a good biomarker for poor health, but it is not a good biomarker for any specific disorder.