We were spending a lot more on AIDS research 20 years ago than on Alzheimer’s today:
https://www.ncbi.nlm.nih.gov/books/NBK222902/
This produced great results for AIDS, which many people thought would never be treatable.
Anyway, medical research is expensive. Considering the number of people who will get Alzheimer’s and the cost to deal with the disease, you would have thought we’d have been spending more on research for the past several decades.
Maybe soon we will all agree that it’s probably worth investing more on research?
https://www.alz.org/get-involved-now/advocate/research-fundi...
Your article says we’ve had a 6x increase. So, we’re approaching 1999 levels not accounting for inflation?
I believe we’re at around $35 billion for AIDS research.
https://www.kff.org/hivaids/fact-sheet/u-s-federal-funding-f...
So AIDS is still 10x greater?
By comparison, we spend closer to $200 billion/year on Alzheimer's treatment. Managing patients who are in severe cognitive decline is not cheap.
We don't understand neurodegeneration yet, and we're probably lumping together hundreds of different disease pathologies under the name "alzheimers," each needing a different treatment approach. If we took the money we've been burning on the same dead end and redirected it to basic research, that might be what best helps crack the code.
I still remember in the early aughts when my professor was part of a research group in 1995 that found a genetic link in Germans from Russia with Alzheimer’s. At the time it was heralded as a huge break through. 25 years later and The needle has barely moved on their research and accomplishments.
In reports published today in the journal Science, researchers say they have isolated a defective Alzheimer’s gene culled from an 8-year-long investigation of several Volga German families, including two from Eastern Washington. Discovery of the gene, and a protein it produces, could speed development of drugs to combat the brain-destroying disorder.
https://www.spokesman.com/stories/1995/aug/18/pioneer-famili...
Seeing your loved ones suffer through Alzheimer’s is one of the most agonizing and depressing things I've had to experience.
That gene, presenilin 2, is part of the amyloid processing complex and plays a role in the amyloid hypothesis (which is highlighted by the news article and the paper itself, https://science.sciencemag.org/content/269/5226/970,) meaning that the very study that this hacker news thread is about, as well as hundreds of other studies and trials, are all investigating this hypothesis. Unfortunately, while the article you've linked says that this discovery helped "solve the mystery of early onset AD," it so turns out that the proposhed mechanism did not live up to scrutiny. Could this protein have different effects (such as a role in calcium ion leakage as later papers suggest)? Perhaps, and it might prove a crucial part of treating alzheimers in the long run, but it doesn't look like that research was in any way overlooked. Research is hard, it's only been a couple decades since new potential mechanisms of action of that gene were identified, and this is a complex disease, but the needle is moving.
HIV and AIDS kill people, and they do so quickly.
There’s also a foothold on how to treat it - whereas for Alzheimer’s we don’t even have an understanding of what actually causes it. Once we know the actual cause I suspect we’ll see research funds skyrocket.
We know how the latter are spread (body fluid contact), and that the virus doesn't live very long outside the body. As a result the precautions needed to ensure I don't personally get it are in general easy to follow. (nothing is perfect but the odds are strongly against me getting it)
Alzheimer's is an unknown. I have no idea if something I'm doing now puts me at risk or not.
I agree with your hypothesis, but saying it out loud seems backwards. In an ideal world, wouldn't we see research funds rise now in order to discover the cause (the hard part) rather than for the treatment (the less hard part).
Please note that I don't speak of an individual research team but of all teams globally combined working on that goal.
I share the cynicism! Early drugs targeted amyloid plaques because it seemed like a good idea. But after so many failures, I can't think of any reason so much time and money is spent on a failed hypothesis other than hoping for a false positive. Because a false positive, even with very modest results, would result in a ridiculously profitable drug given the complete lack of Alzheimer's treatments we currently have.