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Faked Beta-Amyloid Data. What Does It Mean?

Beta-Amyloid has been the dominant explanation for Alzheimer’s for decades. There are a lot of good reasons for thinking that, but every attempt to target it and slow the disease has failed in the clinic...

I think that any ultimate explanation of Alzheimer’s disease is going to have to include beta-amyloid as a big part of the story - but if attacking the disease from that standpoint is going to lead to viable treatments, we sure as hell haven’t been seeing it. We have to put money and effort down on other hypotheses and stop hammering, hammering, hammering on beta-amyloid so much. It isn’t working.

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The brain, Alzheimer’s researchers patiently explain, is hard — harder than the heart, harder even than cancer. While that may be true, it is increasingly apparent that there is another, more disturbing reason for the tragic lack of progress: The most influential researchers have long believed so dogmatically in one theory of Alzheimer’s that they systematically thwarted alternative approaches. Several scientists described those who controlled the Alzheimer’s agenda as “a cabal.”

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The Alzheimer's disease research field has been beset by failed clinical trials and fraud. But researchers remain hopeful that a better understanding of the disease’s broader picture will lead to treatments.

Articles of Interest

Is the Leading Theory About Alzheimer's Wrong?

Yet another failed drug trial has prompted soul-searching about the “amyloid hypothesis.”

The Amyloid Cascade Hypothesis in Alzheimer’s Disease: Should We Change Our Thinking?

The amyloid cascade hypothesis has almost singularly guided AD research, drug development, and clinical trials by targeting Aβ peptides and brain amyloid. Inherited dominant mutations in APP, PS1 or PS2 cause early-onset AD, and yet, after 30 years of research, we know little about the molecular and cellular mechanisms of their action in the development of AD.

You avoided the flames, but I won't. The amyloid beta hypothesis

The amyloid beta hypothesis is the result of a failure to understand that correlation does not imply causation. As a result an entire field of science has been taken over by people who are convinced that the correlation between Alzheimer's and amyloid plaques in the brain is proof of causation. When attempts to treat people on the basis of this theory failed, they doubled down on the theory rather than questioning their reasoning. The result has been decades of failure and suppression of all alternate lines of research.

After amyloid failures, it’s time to take a new tack for treating Alzheimer’s

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One goal is to identify cells that become abnormal long before symptoms of Alzheimer's start to appear. "If we can find the cells where something goes wrong, this would provide a new way to try to treat this disease," Lein says.

Alzheimer’s Disease and the Amyloid Hypothesis: A Rethink is Required

This disconnect between amyloid-beta reduction and clinical outcomes suggests that the role of amyloid-beta in Alzheimer’s disease may not be as straightforward as the amyloid hypothesis proposes. One potential explanation is that amyloid-beta accumulation might be a symptom of the disease, not the cause as I have been discussing for many years. Furthermore, numerous studies have shown that elderly individuals can have substantial amyloid plaques but exhibit no cognitive impairment, challenging the direct link between amyloid and dementia.

Alzheimer’s disease: surprising new theory about what might cause it

We think that it will be important for future trials to focus on the levels of amyloid-beta 42, and whether it is beneficial to increase and restore its levels to normal values instead of targeting it for removal. This could be achieved using proteins similar to amyloid-beta 42 – so-called “protein analogues” – but that clump together less than the natural ones.

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At the heart of this problem is that the field has ossified in decidedly unscientific fashion around the amyloid cascade hypothesis—i.e., the belief that amyloid is toxic and initiates processes disrupting cell function. This has funneled federal, foundation and pharmaceutical/venture capital funding disproportionately into amyloid research despite the fact that the protein’s causal role remains unclear. Indeed, up to 40 percent of people in their 70s have amyloid deposits but normal cognition. It remains a possibility that amyloid deposits are not themselves causal but rather are part of the brain’s injury response.

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Reconsideration of Amyloid Hypothesis and Tau Hypothesis in Alzheimer's Disease

The amyloid hypothesis (also known as the amyloid cascade hypothesis, the Aβ hypothesis, etc.) has been the mainstream explanation for the pathogenesis of AD for over 25 years (Hardy and Allsop, 1991; Selkoe, 1991; Hardy and Higgins, 1992; Hardy and Selkoe, 2002)...

Tau protein—not amyloid—may be key driver of Alzheimer’s symptoms

One of the telltale signs of Alzheimer’s disease (AD) is sticky plaques of ß-amyloid protein, which form around neurons and are thought by a large number of scientists to bog down information processing and kill cells. For more than a decade, however, other researchers have fingered a second protein called tau, found inside brain cells, as a possible culprit. Now, a new imaging study of 10 people with mild AD suggests that tau deposits—not amyloid—are closely linked to symptoms such as memory loss and dementia.

The Amyloid Hypothesis Of Alzheimer’s: Are We On The Right Track?

The amyloid theory faces significant obstacles despite these genetic smoke signals. The discovery that some older individuals without dementia have massive plaque buildup in their brains while others with clinical Alzheimer’s symptoms have little or no plaque was one of them. In fact, a far stronger correlation exists between symptoms getting worse and tau fibril distribution across the brain.

We may finally know what causes Alzheimer’s – and how to stop it

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What causes Alzheimer's? Study puts leading theory to 'ultimate test'

An idea that has propelled Alzheimer's research for more than 30 years is approaching its day of reckoning.