4 ms·

There's a step left out, which is how they know that what happens in the BCO models also happens in real brains in developing fetuses. That might be context kno

by dkarl 2y ago

There's a step left out, which is how they know that what happens in the BCO models also happens in real brains in developing fetuses. That might be context known from previous research, but it isn't explained in the linked article, as far as I can see.

sandworm101 2y ago
They don't. Doing studies on living human fetuses is an admin nightmare. So they use analogues. Black hole physicists also resort to analogues as thier subjects are similarly difficult to manipulate.
- deleted 2y ago
  [deleted]
- zeroonetwothree 2y ago
  Not a good analogy since only one of those is actually present on Earth.
  - sandworm101 2y ago
    But both are untouchable.
    - robwwilliams 2y ago
      You can image and get in vivo estimates of brain volume. Here is a paper that does so: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8583264/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8583264/
- nathan_compton 2y ago
  I would hope that the epistemological status of medical discoveries exceeds somewhat that of knowledge of black holes.
mumblemumble 2y ago
I don't think you need that specific interpretation to decide that this work reveals something important. We have a phenotypic difference that leads to a big in vitro difference, and it's not a huge jump to infer that that would also lead to an in vivo difference, even if the in vivo presentation is unknown, or the exact details of the presentation aren't the same. Here's the conclusions section from the research paper this article is summarizing: By embryogenesis, the biological bases of two subtypes of ASD social and brain development - profound autism and mild autism — are already present and measurable and involve dysregulated cell proliferation and accelerated neurogenesis and growth. The larger the embryonic BCO size in ASD, the more severe the toddler’s social symptoms and the more reduced the social attention, language ability, and IQ, and the more atypical the growth of social and language brain regions. This is not making any huge logical jumps that I noticed. All it's saying is they found a strong correlation. And the researchers seem to be well aware that there are still dots to connect. In the limitations section, it explicitly points out more-or-less the very thing that the researchers are being accused of not thinking about in this HN thread: The genetic causes and cellular consequences of decreased Ndel1 activity and expression correlated with ASD BCOs enlargement remain to be specified. A limitation of most previous ASD patient-derived iPSC-based models is lack of within-subject statistical linkage of ASD molecular and cellular findings with variation in ASD social phenotypes. Without this, future ASD iPSC reports will continue to have limited impact on our understanding of the genetic, molecular and cellular mechanisms that cause the development and variation in the central feature of ASD: social affect and communication. Which brings us to an important thing about interpreting popular science literature: it's unwise to assume that what's in the popularization of the research accurately reflects everything the scientists who published the work think or know. Attempting to eliminate these kinds of details is one of the primary goals of science journalism. For better or for worse. https://molecularautism.biomedcentral.com/articles/10.1186/s13229-024-00602-8 https://molecularautism.biomedcentral.com/articles/10.1186/s...
- dkarl 2y ago
  I don't think the other poster was objecting to the excitement about this being a potentially important discovery, or criticizing the research or the researchers. They are objecting to the way the linked article presents it, specifically its claim that "Courchesne and Muotri have established that brain overgrowth begins in the womb." As readers of this article we can fill in the blanks and imagine that there might be a well-understood and well-founded way to extrapolate observations of these BCO samples to fetal brain development, but we can equally well imagine that this extrapolation might be tricky or unreliable. So as lay readers we're left to guess which mistake the author made: did they overstate the conclusion based on a bad assumption, or, after already explaining so much about the research and connecting so many dots for the reader, did they forget to explain why we can confidently draw conclusions about real fetal brains from these in vitro models? Obviously the second is more forgivable, but it's annoying either way.

by dkarl 2y ago

sandworm101 2y ago

They don't. Doing studies on living human fetuses is an admin nightmare. So they use analogues. Black hole physicists also resort to analogues as thier subjects are similarly difficult to manipulate.

deleted 2y ago
[deleted]
zeroonetwothree 2y ago
Not a good analogy since only one of those is actually present on Earth.
- sandworm101 2y ago
  But both are untouchable.
  - robwwilliams 2y ago
    You can image and get in vivo estimates of brain volume. Here is a paper that does so: https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8583264/ https://www.ncbi.nlm.nih.gov/pmc/articles/PMC8583264/
nathan_compton 2y ago
I would hope that the epistemological status of medical discoveries exceeds somewhat that of knowledge of black holes.

mumblemumble 2y ago

I don't think you need that specific interpretation to decide that this work reveals something important. We have a phenotypic difference that leads to a big in vitro difference, and it's not a huge jump to infer that that would also lead to an in vivo difference, even if the in vivo presentation is unknown, or the exact details of the presentation aren't the same. Here's the conclusions section from the research paper this article is summarizing: By embryogenesis, the biological bases of two subtypes of ASD social and brain development - profound autism and mild autism — are already present and measurable and involve dysregulated cell proliferation and accelerated neurogenesis and growth. The larger the embryonic BCO size in ASD, the more severe the toddler’s social symptoms and the more reduced the social attention, language ability, and IQ, and the more atypical the growth of social and language brain regions. This is not making any huge logical jumps that I noticed. All it's saying is they found a strong correlation. And the researchers seem to be well aware that there are still dots to connect. In the limitations section, it explicitly points out more-or-less the very thing that the researchers are being accused of not thinking about in this HN thread: The genetic causes and cellular consequences of decreased Ndel1 activity and expression correlated with ASD BCOs enlargement remain to be specified. A limitation of most previous ASD patient-derived iPSC-based models is lack of within-subject statistical linkage of ASD molecular and cellular findings with variation in ASD social phenotypes. Without this, future ASD iPSC reports will continue to have limited impact on our understanding of the genetic, molecular and cellular mechanisms that cause the development and variation in the central feature of ASD: social affect and communication. Which brings us to an important thing about interpreting popular science literature: it's unwise to assume that what's in the popularization of the research accurately reflects everything the scientists who published the work think or know. Attempting to eliminate these kinds of details is one of the primary goals of science journalism. For better or for worse. https://molecularautism.biomedcentral.com/articles/10.1186/s13229-024-00602-8 https://molecularautism.biomedcentral.com/articles/10.1186/s...

dkarl 2y ago
I don't think the other poster was objecting to the excitement about this being a potentially important discovery, or criticizing the research or the researchers. They are objecting to the way the linked article presents it, specifically its claim that "Courchesne and Muotri have established that brain overgrowth begins in the womb." As readers of this article we can fill in the blanks and imagine that there might be a well-understood and well-founded way to extrapolate observations of these BCO samples to fetal brain development, but we can equally well imagine that this extrapolation might be tricky or unreliable. So as lay readers we're left to guess which mistake the author made: did they overstate the conclusion based on a bad assumption, or, after already explaining so much about the research and connecting so many dots for the reader, did they forget to explain why we can confidently draw conclusions about real fetal brains from these in vitro models? Obviously the second is more forgivable, but it's annoying either way.