5 ms·

I’m skeptical, though I must admit that I’m not a subject matter expert. The disruption of serotonergic pathways probably isn’t something that can be amended b

I’m skeptical, though I must admit that I’m not a subject matter expert. The disruption of serotonergic pathways probably isn’t something that can be amended by a serotonergic therapy. I’d actually predict that individuals with Alzheimer’s would experience a diminished effect when taking LSD. My bias here is more broad. I’m of the belief that the cure to Alzheimer’s is more likely biological than it is chemical. Not overlooking the interoperability of these two things, but rather suggesting that it’s probably a problem that requires a more sophisticated treatment than purely consuming a drug. That said, I’m very excited to see microdosing being studied and interested in the outcomes of this trial, whatever they may be. Certainly, the results here could tell us something we haven’t yet discovered about LSD or Alzheimer’s, even if there is no therapeutic application in this case.

MagnumPIG 7y ago
With regard to treatment, what are you basing your belief on? Plenty of diseases can be halted or cured with chemicals.
- ekianjo 7y ago
  The numerous trials with "chemicals" that had absolutely no effect on Alzheimer so far. It is not for lack of trying at this stage.
- bransonf 7y ago
  Of the research I’ve read, many scientists suggest that it’s the accumulation of plaques that cause Alzheimer’s.[0] There’s uncertainty as to what protein is responsible for the degenerative effects.[1] My bias exists for the fact that I believe the cure to Alzheimer’s is removing or preventing the development of this plaque. At least I’ve been lead to believe this is among the most promising cures.[2] Amyloid protein is particularly tricky because it’s insoluble. I don’t think we could develop a purely chemical solution for the fact that it would likely be destructive to our own biology. And I think both gene expression and enzyme production are unlikely to be able to changed with just a drug. [0] https://www.sciencedaily.com/releases/2018/03/180326161000.htm https://www.sciencedaily.com/releases/2018/03/180326161000.h... [1] https://www.sciencemag.org/news/2016/05/tau-protein-not-amyloid-may-be-key-driver-alzheimer-s-symptoms https://www.sciencemag.org/news/2016/05/tau-protein-not-amyl... [2] https://rupress.org/jem/article/215/3/927/42616/BACE1-deletion-in-the-adult-mouse-reverses https://rupress.org/jem/article/215/3/927/42616/BACE1-deleti...
  - CuriouslyC 7y ago
    The beta amyloid theory is pretty tired at this point since the correlation between plaques and Alzheimer's is only moderate. Imo Alzheimer's is probably more related to the brain falling into dysdunctional, self reinforcing patterns of synaptic connectivity. Neural plaques might exacerbate this problem by disrupting connectivity, but clearly the brains of many people with plaques learn to route around this damage to retain functionality.
    - bransonf 7y ago
      > self reinforcing patterns of synaptic connectivity Any sources for this? I’d be very interested to read the literature on this.
      - CuriouslyC 7y ago
        https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207354/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207354/ Just a jumping off point review on the weakness of the amyloid theory. The connectome dysregulation theory is my own, it hasn't appeared in the scientific literature as of yet due to our inability to perform fine mapping of synaptic connections without microtoming a cadaver brain.
        kortex 7y ago
        That's a cool theory. The brain tries pretty hard to maintain criticality (hard as in, disruptions cause it to return to that setpoint quickly). It's possible that inability to recover or maintain optimal processing criticality can lead to corruption of the connectome. https://www.sciencedaily.com/releases/2019/10/191007113314.htm https://www.sciencedaily.com/releases/2019/10/191007113314.h...
  - shakil 7y ago
    See this case of a Colombian woman whose brain is full of the amyloid plaque but she is demntia free due to a genetic mutation https://www.sciencemag.org/news/2019/11/colombian-woman-s-genes-offer-new-clues-staving-alzheimer-s https://www.sciencemag.org/news/2019/11/colombian-woman-s-ge...

MagnumPIG 7y ago

With regard to treatment, what are you basing your belief on? Plenty of diseases can be halted or cured with chemicals.

ekianjo 7y ago
The numerous trials with "chemicals" that had absolutely no effect on Alzheimer so far. It is not for lack of trying at this stage.
bransonf 7y ago
Of the research I’ve read, many scientists suggest that it’s the accumulation of plaques that cause Alzheimer’s.[0] There’s uncertainty as to what protein is responsible for the degenerative effects.[1] My bias exists for the fact that I believe the cure to Alzheimer’s is removing or preventing the development of this plaque. At least I’ve been lead to believe this is among the most promising cures.[2] Amyloid protein is particularly tricky because it’s insoluble. I don’t think we could develop a purely chemical solution for the fact that it would likely be destructive to our own biology. And I think both gene expression and enzyme production are unlikely to be able to changed with just a drug. [0] https://www.sciencedaily.com/releases/2018/03/180326161000.htm https://www.sciencedaily.com/releases/2018/03/180326161000.h... [1] https://www.sciencemag.org/news/2016/05/tau-protein-not-amyloid-may-be-key-driver-alzheimer-s-symptoms https://www.sciencemag.org/news/2016/05/tau-protein-not-amyl... [2] https://rupress.org/jem/article/215/3/927/42616/BACE1-deletion-in-the-adult-mouse-reverses https://rupress.org/jem/article/215/3/927/42616/BACE1-deleti...
- CuriouslyC 7y ago
  The beta amyloid theory is pretty tired at this point since the correlation between plaques and Alzheimer's is only moderate. Imo Alzheimer's is probably more related to the brain falling into dysdunctional, self reinforcing patterns of synaptic connectivity. Neural plaques might exacerbate this problem by disrupting connectivity, but clearly the brains of many people with plaques learn to route around this damage to retain functionality.
  - bransonf 7y ago
    > self reinforcing patterns of synaptic connectivity Any sources for this? I’d be very interested to read the literature on this.
    - CuriouslyC 7y ago
      https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207354/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC4207354/ Just a jumping off point review on the weakness of the amyloid theory. The connectome dysregulation theory is my own, it hasn't appeared in the scientific literature as of yet due to our inability to perform fine mapping of synaptic connections without microtoming a cadaver brain.
      - kortex 7y ago
        That's a cool theory. The brain tries pretty hard to maintain criticality (hard as in, disruptions cause it to return to that setpoint quickly). It's possible that inability to recover or maintain optimal processing criticality can lead to corruption of the connectome. https://www.sciencedaily.com/releases/2019/10/191007113314.htm https://www.sciencedaily.com/releases/2019/10/191007113314.h...
- shakil 7y ago
  See this case of a Colombian woman whose brain is full of the amyloid plaque but she is demntia free due to a genetic mutation https://www.sciencemag.org/news/2019/11/colombian-woman-s-genes-offer-new-clues-staving-alzheimer-s https://www.sciencemag.org/news/2019/11/colombian-woman-s-ge...