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I can’t claim to know much about this, but as someone who recently suffered from possibly temporary amyloidosis-like symptoms, I’ve had to research this a lot recently.

Basically, amyloids have been known for centuries as e.g. white stuff that collects in spleens and recently research on dementia has turned to amyloids as one of the precursors of one of the types of Alzheimer’s. It’s not yet clear if every case has amyloid involvement or if clearing amyloids can resolve the condition without any side effects yet, in particular there’s been reported brain shrinkage.

https://en.m.wikipedia.org/wiki/Amyloid_beta talks about the thing floating around your body in more detail.

I can’t say I’m an expert at any of this though. I’ve mostly looked at this from an AA amyloidosis perspective rather than an Altzheimer’s one.

We actually already have a test for the presence of amyloids - SAA blood tests commonly used to diagnose infection in horses and cats. Other creatures, including humans, can also measure C Reactive Protein, but both CRP and SAA are measures of stress or inflammation associated with bacterial infection. Your body routinely gets rid of amyloids it might produce, which is part of why it’s said people with AA amyloidosis recover when the underlying cause is treated, I think. But it’s unclear how well we can recover long-term and amyloids and biofilms are still active research areas.

All I can say is that for my amyloidosis-like symptoms, taking vitamin C regularly helps my thinking and the occasional high dose of vitamin A appears to temporarily reverse some of the amyloid-induced nerve damage. But I should also clarify I’m still awaiting test results to determine if I have amyloids and also my condition improves with antibiotics which means vitamin A and C might be interfering with bacteria (where biofilm = amyloids) rather than with the amyloid fibrils on their own.




Wasnt the base theory, that some viruses damage cells, that then do not become cancerous, but produce useless protein crap, that spills everywhere? Basically slow death, by spam every cellular division?


Are you talking about cellular senescence? Those cells don’t divide. They produce inflammatory proteins, aka senescence-associated secretary phenotype. More senescent cells in ageing, but no direct link AFAIK.


Yes, yes, that was it. Garbage slowly clogging the maintenance functions, building up other toxic substances, like plastic bags clogging a chemical plant over time..

And it does not have to be directly.. it just has to tilt the chemical environment slowly, but steadily towards something bad downstream.


It is clear that clearing the amyloids does not relieve one from the symptoms of dementia, or stop them. See Aducanumab, and the amyloid hypothesis nature article.




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