How an outsider bucked prevailing Alzheimer's theory, clawed for validation

One of things I like about the Howard Hughes Medical Institute (HHMI) is that they find great scientists and just fund them. The scientists can research whatever they want as long as they keep producing. I always wondered if a hybrid approach to funding would work well at the government level. The current, permission-based process would remain in place for new researchers to prove themselves, and then an HHMI-style process for researchers who have proven themselves. There would be checks in place and if the funded researchers stop performing then they have to go back to the normal process. There are several details that would have to be worked out to guard against politics, etc. I think this may overcome the government agencies tendency to reject truly new ideas especially when they contradict the prevailing theory.

This isn&#x27;t a particularly surprising story considering the history of science. To give an example of how this sort of thing played out historically, Marshall Nirenberg was basically persona non grata (or at least dutifully ignored) at many scientific conferences prior to his postdoc&#x27;s discovery of the codon for phenylalanine. At the time, he was working at the NIH, which was considered very low prestige by many contemporary scientists. Somewhat fortuitously, Francis Crick heard a lecture by Nirenberg at a conference in 1961 and considered it good enough to bring to the attention of the other key players of the day, and Nirenberg was elevated from obscurity to stardom. For whatever reason, Nirenberg&#x27;s postdoc never really achieved stardom, despite being the individual who <i>actually</i> made the discovery.<p>For more information:<p><a href="https:&#x2F;&#x2F;www.telegraph.co.uk&#x2F;news&#x2F;science&#x2F;science-news&#x2F;8546830&#x2F;Genes-and-DNA-meet-the-first-man-to-read-the-book-of-life.html" rel="nofollow">https:&#x2F;&#x2F;www.telegraph.co.uk&#x2F;news&#x2F;science&#x2F;science-news&#x2F;854683...</a>

Amyloid-beta is associated with sleep deprivation. This new research could suggest that sleep is an essential component of the immune system.<p><i>If so, then the plaques it forms might be the brain’s last-ditch effort to protect itself from microbes, a sort of Spider-Man silk that binds up pathogens to keep them from damaging the brain. Maybe they save the brain from pathogens in the short term only to themselves prove toxic over the long term.</i><p>I really like the thinking here.<p>Similarly: In people with CF, calcium and glutathione build up in the cells. High levels of calcium are associated with cell death, so much of the CF community believes calcium is harmful.<p>I believe the calcium and glutathione are desperate efforts to buffer the cell in the face of deranged cell chemistry. I believe the high calcium is indicative of other things being really bad and the body trying desperately to compensate.<p>If this guy wants another outside-the-box research project, there you go. I would love to see that looked into.<p>Edit: Is it me, or does the article actually switch from saying <i>amyloid-beta</i> to saying <i>beta-amyloid</i> midway through?<p><i>This month, however, he got an unheard-of email from NIH: The agency had found some extra money lying around in its budget. Would he please respond to the reviewers and resubmit his proposal? An over-the-moon Moir did. He expects to hear back in a few weeks.</i><p>Yay! I hope he gets it.

This seems to be referencing the path to mainstream exposure for the infectious theory of Alzheimer&#x27;s. Prior discussions (not the same link) on HN, posted for reference because they touch on the past research that was previously posted here:<p><a href="https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=18306381" rel="nofollow">https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=18306381</a> (this one&#x27;s a comment I made associating the cortisol&#x2F;Alz risk to the microbial Alz connection; it&#x27;s nothing more than a hypothesis)<p><a href="https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17446016" rel="nofollow">https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17446016</a><p><a href="https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17540512" rel="nofollow">https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17540512</a><p><a href="https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17540094" rel="nofollow">https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=17540094</a> (this is the parent link for the antiviral risk reduction study -- a good read, comments and source article)<p>There&#x27;s a decent amount of reading when scholar-googling:<p><a href="https:&#x2F;&#x2F;scholar.google.com&#x2F;scholar?q=hsv1+alzheimers" rel="nofollow">https:&#x2F;&#x2F;scholar.google.com&#x2F;scholar?q=hsv1+alzheimers</a><p>Moir&#x27;s paper specifically: the relationship between β-Amyloid and viruses in the brain:<p><a href="https:&#x2F;&#x2F;www.cell.com&#x2F;neuron&#x2F;fulltext&#x2F;S0896-6273(18)30526-9" rel="nofollow">https:&#x2F;&#x2F;www.cell.com&#x2F;neuron&#x2F;fulltext&#x2F;S0896-6273(18)30526-9</a> (study link)<p>There&#x27;s also research pointing to sleep&#x27;s function as helping clear out plaques such as beta-amyloid.<p><a href="https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=16026655" rel="nofollow">https:&#x2F;&#x2F;news.ycombinator.com&#x2F;item?id=16026655</a><p>Finally, there&#x27;s at least a bit of research pointing to boosted susceptibility of herpes viral infections when carrying ApoE4:<p><a href="https:&#x2F;&#x2F;scholar.google.com&#x2F;scholar?q=hsv1+apoe4" rel="nofollow">https:&#x2F;&#x2F;scholar.google.com&#x2F;scholar?q=hsv1+apoe4</a><p>The novel conclusion from all of this, which I suspect is being actively investigated, is that there&#x27;s a potentially complicated interplay of an enhanced viral infection (HSV&#x2F;HHV enabled by ApoE4) + evolutionary defense going into overdrive (β-Amyloid) + (potentially) sleep deprivation keeping the body from clearing out the residue -&gt; disease.<p>---<p>I&#x27;m particularly motivated to track this research because of its prevalence in my family background and because, from what I can tell, I&#x27;ve thus far managed to avoid the environmental trigger-pull. I can already tell you I&#x27;ll probably go on (val)acyclovir lifetime if I&#x27;m ever diagnosed with any particular strain, as it looks like active infection, with outbreaks, is what&#x27;s likely to act as the first domino to tip.

This all makes sense. APOE literally carries viruses around the body : <a href="https:&#x2F;&#x2F;bit.ly&#x2F;2oRVFSr" rel="nofollow">https:&#x2F;&#x2F;bit.ly&#x2F;2oRVFSr</a>

&gt; Complaints about being denied NIH funding are as common among biomedical researchers as spilled test tubes after a Saturday night lab kegger.<p>Comedy in science writing?

&gt; Complaints about being denied NIH funding are as common among biomedical researchers as spilled test tubes after a Saturday night lab kegger<p>Is this supposed to mean complaints are common?