It's been some years for me so things might have changed, but no tech was allowed into the exam rooms, except for calculators in some subjects. Everything was done by pen and paper.

Comments URL: https://news.ycombinator.com/item?id=48128349

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It is assumed that students will attempt to cheat, so exams are designed so that cheating is not a viable strategy to obtain high grades. So-called invigilators also patrol the exam room and will report any violations.

We have to take it on faith that they did in fact specifically set out to determine if egg consumption was associated with Alzheimer's disease...

A quick search shows that other studies both do [0] and do not [1] link egg consumption with Alzheimer's disease.

[0] https://pubmed.ncbi.nlm.nih.gov/38782209/; https://pubmed.ncbi.nlm.nih.gov/31360988/

[1] https://pubmed.ncbi.nlm.nih.gov/28052883/; https://pubmed.ncbi.nlm.nih.gov/33561122/

From the actual study, which is free to read [0]:

>Dietary intake was assessed at baseline using a validated, self-administered FFQ that included >200 food items

So out of 200 potential associations, eggs were the winner? See this famous xkcd: Green jelly beans linked to acne.[1]

[0] https://www.sciencedirect.com/science/article/pii/S002231662...

[1] https://www.explainxkcd.com/wiki/index.php/882:_Significant

https://www.usgs.gov/media/images/land-subsidence-san-joaqui...

The exposure time of these kite photographs must have been quite short, given the obvious instability of the platform. They're very detailed, nonetheless.

What are the practical consequences of this today, and what is being done to remedy this?

For the GLP-1 strategy, Table 1 in the above paper shows that all drugs were clearly effective. Some were better than others.

For the amyloid strategy, only some of the drugs were effective, and that efficacy was very weak, even when all the drugs removed amyloid. This brings into question the hypothesis that removing amyloid would alleviate AD, i.e. the slender benefits of Lecanemab might not be caused by amyloid removal. The same cannot be said for the GLP-1 receptor agonists.

The point about the anti-amyloid trials is that they all succeeded in removing amyloid. But they did not improve cognition, and only some resulted in a slightly slower rate of decline in cognition (people still declined).

[0] https://pubmed.ncbi.nlm.nih.gov/39841962/

>Forty-seven RCTs were included, with a combined cohort of 23,244 patients. GLP-1 RAs demonstrated a mean weight reduction of -4.57 kg (95% CI -5.35 to -3.78), mean BMI reduction of -2.07 kg/m2 (95% CI -2.53 to -1.62), and mean waist circumference reduction of -4.55 cm (95% CI -5.72 to -3.38) compared with placebo.

It's possible, of course, that some methods of targeting amyloid might work where others failed. But even those that claim success (Donanemab and Lecanemab) have a very modest benefit.

It doesn't ask whether amyloid is causative of the disease.

Trials are currently ongoing. The results should start trickling out in a few years...

As to the trials specifically for Lecanemab and Donanemab, the benefits are not claimed to be either strong or large, even by those who support it. The current support these receive is more aligned with the concept that an improved targeting of Aβ amyloid might improve outcomes. This remains to be demonstrated.

[0] https://www.cochrane.org/evidence/CD016297_are-medicines-ant...

Alzheimer's disease may occur either due to inherited mutations in the genes for APP or presenilin, in which case it can occur as young as 40 yrs old. Or it may occur "sporadically" in those over 65yrs old. The brain pathology of both is similar. Notably, amyloid is derived from APP in part by the action of presenilin, which cuts the APP protein to release the amyloid peptide (Aβ).

Currently, the amyloid hypothesis is the only known way to reconcile the similarity of pathology (for both amyloid and tau) between early onset inherited AD caused by mutations in either APP or presenilin, and later onset sporadic disease. Furthermore, all the mutations in APP that cause Alzheimer's disease are located within or adjacent to the region that corresponds to Aβ amyloid, and not in the remaining 95% of the molecule.

Until another way of unifying these observations is found, the amyloid hypothesis will always find supporters.

It frequently hosts journalists, politicians, lawyers, etc, who have had successful careers outside of academia and who may have no academic qualifications other than an undergraduate degree, and sometimes no degree at all.