New study ties tau production to amyloid burden

[NF52]

From MedPageToday, some more evidence from 24 human subjects with either mild AD or cognitively normal, that amyloid increases correlate with increased tau production in spinal fluid samples. Whether the amyloid causes the increased tau is not proven, but it does suggest that reducing amyloid, even assuming that it is only one of many proximate causes of AD progression, is a good target. And that learning more about different types of tau, which reproduce at different rates, could lead to anti-tau therapies.

As the nurse practitioner in the Generations Trial told me on Monday, "We're pretty sure than no one drug is going to solve everything. It's going to be a combination of therapies."

.Do Amyloid Plaques Drive Tau Deposition? New study ties tau production to amyloid burden

In CSF samples from 24 participants, including patients with mild Alzheimer's disease and cognitively normal controls, stable isotope labeling kinetics (SILK) analysis showed a direct correlation between the amount of amyloid and the amount of tau. This held true whether patients showed symptoms of Alzheimer's disease or not: if there were amyloid plaques, there was increased production of soluble tau.

"We knew that people who had plaques typically had elevated levels of soluble tau," Bateman said in a statement. "What we didn't know was why. This explains the why: the presence of amyloid increases the production of tau."

https://www.medpagetoday.com/neurology/ ... ease/71910

[cwicker]

I'm confused by the conclusion. There is an association, meaning the presence of soluble tau can also be causing the amyloid, correct? To me, the conclusion that amyloid causes the tau continues to lead us down the amyloid causing Alzheimer's hypothesis. A hypothesis which seems flawed looking at the scientific literature.

[Dan Parkie 234]

Thanks NF52,
That's exactly the type of peer reviewed literature I have been hoping to find.
Dan

[NF52]

Thanks NF52,
That's exactly the type of peer reviewed literature I have been hoping to find.
Dan

Thanks, Dan! Peer-reviewed literature can be confusing, especially for a non-scientist like me, so I've been trying to educate myself by using Google Scholar as a source for searches, following links of articles that Pub Med and other sites show as "similar articles" or "Cited by". Even rabbit holes can expand my grasp of the complexities!

If you're looking for a relatively brief and easy-to-read resource on how to get the most out of things like "confidence intervals" and "double-blinded randomization", as well as looking differently at whether studies had 25 volunteers or a population-based cohort, I recommend Basics for Evaluating Medical Research Studies: A Simplified Approach, by a group in the UK that teaches doctors and others how to critically assess studies. (Got mine on Kindle.)

Feel free to check the Search function in the upper right 3-dots if there are particular topics you're hoping to explore, or shoot me a Private Message if you have questions on how to use Google Scholar.

I see that you're a retired social worker. I had many colleagues in special education who were great social workers and wise friends. They taught me that understanding family and social systems made understanding an individual student much easier. Recognizing the strengths in every individual, regardless of external labels of disability, illness or impairment, makes supporting the individual's right to make meaningful choices, even if those seem mis-guided by my values. That's why this supportive community is a great for for people like you and me, and why your experience and wisdom in already supporting several others on this site is appreciated! We need that passion for sharing and self-determination in the fields of genetics, chronic health conditions, aging-in-place choices, and end-of-life choices.

[Dan Parkie 234]

Here's another article about amyloid and tau: //www.nature.com/articles/s41598-018-23041-x
Thanks for the kind words about social work.
Dan

[NF52]

Hi Dan!
Thanks for linking to another article on tau and amyloid.

To get links to show on this site, you have to nudge the software along: I go to the tab bar on my Mac, highlight the web address & copy/paste it. Then I go to the shaded choices right above the draft reply page and lick on URL-located to the left of the white "Normal" box. [if you're on Quick Reply, just go below that screen and click on Full Editor and Preview.] It pulls up the code in the php.bb software that makes the URL show up as it would on a Google or Word doc.

18F-AV-1451 in Parkinson’s Disease with and without dementia and in Dementia with Lewy Bodies
https://www.nature.com/articles/s41598-018-23041-x

I think it's fascinating to see that many studies are still in the "here's what it seems to mean when this area lights up on a PET scan". While it would be helpful to fast-forward to when the pathways and functions of the brain in AD, PD, etc are so well understood that upstream interventions can be personalized with one PET scan, I take comfort that those images I provide in a clinical study of "normal but at high risk people" will advance the science faster.

Mixed pathologies of α-synuclein, β-amyloid and tau are relatively common in Parkinson’s disease (PD) and Dementia with Lewy Bodies (DLB).... In conclusion DLB patients have increased parietal 18F-AV-1451 uptake. Increased parietal tau is associated with executive impairment in patients with synucleinopathies, while decreased uptake in the substantia nigra is associated with parkinsonism.