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Is the key to Alzheimer’s disease lurking, overlooked, in the 100,000-plus scientific papers that have been published on this disease over the last century?

A Texas businessman who lost family members to dementia thinks so, and on Monday he announced that there’s $4 million waiting for the people who find it: Prizes of up to $2 million will be awarded to those who comb the scientific literature, extract the key findings, and synthesize them into one simple explanation of the disease, said James Truchard, 75, an electrical engineer who recently retired as CEO of National Instruments, which he co-founded in 1976.


“The pieces of this puzzle are out there,” Truchard told STAT. ApoE4, beta-amyloid, tau, microbes, inflammation, metabolism, FOXP3, and APP are only some of the genes, peptides, and biological processes that have been identified as contributing to Alzheimer’s, but they have not been synthesized into a “grand unified theory” of Alzheimer’s that might lead to a treatment or cure, he said: “I’m hoping there’s some genius out there who will put them together.”

National Instruments
James Truchard National Instruments

The Oskar Fischer Prizes, announced at the annual meeting of the Society for Neuroscience, will be administered by the University of Texas at San Antonio College of Sciences. It’s not clear what the criteria will be for winning either the $2 million top prize or the runners-up (two second-place prizes of $500,000 each and four third-place prizes of $250,000), such as whether what seems like a brilliant synthesis on paper will need to be confirmed experimentally.

“All of the specifics related to the challenge and the judging haven’t been determined yet,” said a UT spokesperson.


Despite that ambiguity, some leading Alzheimer’s researchers who were told about the new prizes by STAT expressed cautious enthusiasm.

“I guess one never knows,” said Dr. Howard Fillit, executive director and chief science officer of the Alzheimer’s Drug Discovery Foundation. “It does seem a bit risky in achieving the goal of finding a theory that completely explains the disease, but the actual weaving of the literature into a theory shouldn’t be that hard.”

“I do think the answer is in the composite literature and this is a brilliant idea!” said Rudy Tanzi of Massachusetts General Hospital, a pioneer in the search for Alzheimer’s-related genes who has recently been investigating the role of the brain’s microbiome and inflammation in the disease.

The prizes are meant to reward an individual, not fund research, although the winners could use it for that or any other purpose. Dangling a financial lure, Truchard said, “seems like a good way to get an answer on the table.”

Another Alzheimer’s prize, $1 million for “providing proof that an infectious agent is the root cause” of the disease, was announced in January. Dr. Leslie Norins, who established that prize, said the fact “that anybody is giving millions for anything related to Alzheimer’s except the tired old ‘amyloid and tau’ is news in itself,” but asked, “what the heck is the deliverable? Surely it’s not just a master compendium of all journals papers on Alzheimer’s.”

Fischer, a Czech neuroscientist who lived from 1876 to 1942, identified plaques and tangles in the brains of 16 people with dementia. He published his findings in 1907, the year Alois Alzheimer described a patient with an early onset form of the disease that would soon be named for him. In 1939, the Nazis forced Fischer out of his university professorship; he died in a concentration camp. His work was overlooked for decades, one of many examples of published studies being ignored or lost — as Truchard believes the key to curing Alzheimer’s disease has been.

The call for proposals for the prizes will be available in February.

    • Rob, Thanks for posting this article. This is a very detailed look at inflammation and neurodegenerative diseases. At the end of the paper they discuss outstanding questions which need to be answered. They have not found out what causes the inflammation. “What is/are the mechanism(s) for transition from the acute (protective) to chronic (pernicious) phase of inflammation? The transition between these two phases would appear an ideal therapeutic target.” Aluminum is a cause of this inflammation.

  • Competition never hurts. It’s pushes people to maybe look at this differently and a little harder. As long as the research keeps happening it can’t hurt. Been reading Race for the Mind by Daniel Welch, it’s interesting as he looks at all the aspects of the disease, not just at the patient with it. It’s a great read on the disease. His proceeds from the book is all being donated to research as well, so a book with a purpose!

  • There is an effective treatment for Alzheimer’s available now. I have been taking the anti-inflammatory drug montelukast (brand name Singulair) for almost 3 years, and my extreme mental fatigue and occasional confusion disappeared after the first week, and I am completely back to normal. I take one 10 mg tablet three times a day. A clinical trial for this drug for Alzheimer’s has just begun in Canada under the supervision of the Canadian government and the trial is also registered with the FDA. Google the words montelukast Alzheimer’s for more information.

  • We should be clear that any “hypothesis” that comes out from a synthesis of the published literature will need to content with two problems: a) there is a huge publication bias in the literature, so any emerging hypothesis will likely be biased and b) whatever emerges from this exercise will need to be empirically tested. A hypothesis is not a solution..but its a necessary prelude to developing effective therapeutics.

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