Ethics in Medicine

Alzheimer’s : Tragedy of Alzheimer Fraud Research

Kristen Sparrow • January 31, 2025

I’ve touched on this controversy and tragedy in the world of Alzheimer’s research, here

here

here and in my book, Radical Resilience.

This editorial is from the NY Times from a scientist who helped uncover the faulty science.  He’s also the author of a new book.  The comment section is particularly interesting.  Many thoughtful comments, and there was at least one dissenting opinion.

Summary of the Editorial: The Crisis in Alzheimer’s Research

For decades, Alzheimer’s research has been plagued by fraudulent data, manipulated findings, and perverse incentives that have distorted the field. Despite billions of dollars in funding, no treatment has successfully halted or reversed cognitive decline, and the field has been dominated by the flawed amyloid hypothesis—the idea that amyloid plaques cause Alzheimer’s. This unproven theory has driven scientific groupthink, attracting funding, corporate investment, and career advancement opportunities, even as its failures mount.

1. Perverse Incentives in Research
The intense competition for funding and recognition has incentivized misconduct. Researchers who support prevailing theories—like the amyloid hypothesis—gain easier access to grants, promotions, and lucrative pharmaceutical partnerships. Fraudulent studies, like those from Dr. Eliezer Masliah and others, have shaped the field despite containing manipulated images and falsified data. Nearly 600 dubious studies have been cited over 80,000 times, warping scientific discourse. The financial stakes are enormous—pharmaceutical companies continue to push anti-amyloid drugs that yield negligible benefits but cost patients tens of thousands of dollars annually. Meanwhile, fraudulent research has laid the foundation for patents and drug trials, further misleading the field.

2. The Role of Tau Proteins in Alzheimer’s
While amyloid plaques have dominated Alzheimer’s research, tau proteins—which accumulate inside neurons—may play a more significant role in the disease. Some researchers argue that tau tangles disrupt neural function long before amyloid plaques appear. However, because funding and career success have been tied to amyloid research, alternative hypotheses, including tau-targeting treatments, have been underfunded. Recent studies suggest that brain inflammation, infections, and even metabolic dysfunction could be key drivers of neurodegeneration, but these avenues remain underexplored due to entrenched biases.

The editorial underscores the urgent need for scientific integrity, diversified research, and a break from amyloid-centric dogma to find effective Alzheimer’s treatments.