“The scientific method” — it’s just not used, e.g. in Alzheimer’s Disease
Posted by Henry Bauer on 2014/07/17
Alzheimer’s disease is one of the dysfunctional knowledge monopolies mentioned in my book, Dogmatism in Science and Medicine (pp. 108-9).
Decades-old dogma takes the cause of the disease to be the build-up in the brain of plaques of amyloid protein. However, a mass of actual evidence indicates that theory to be wrong: there have been “hundreds of experiments casting doubt on the neurotoxicity of amyloid”; drugs and vaccines that act against the plaque have been ineffective; amyloid injected into brains of mice caused no symptoms. Yet researchers find it very difficult to get their evidence for other causes of Alzheimer’s published or to get research support for their work.
Rationalizations that try to prop up the amyloid theory are feeble and far-fetched, as illustrated by a fairly recent paean to a “breakthrough”:
“New imaging shows Alzheimer’s unfolding in live brains” (Andy Coghlan, New Scientist, 18 September 2013):
“The two major brain abnormalities that underlie Alzheimer’s disease can now be viewed simultaneously in brain scans while people are still alive”. Amyloid plaque has been observable since 2005 by PET (positron emission tomography), but now one can also observe “tau tangles”, and “tau lesions are known to be more intimately associated with neuronal loss than plaques . . . . tau tangles accumulate first in the hippocampus — the brain’s memory centre — at a time when the plaques are already widespread. . . . Previous research has shown that the tangles rapidly kill neurons and trigger behavioural changes. . . . [The new] images suggest that the plaques are themselves harmless, but help to advance disease by spreading the tau tangles from the hippocampus to other brain regions” [emphases added].
Note first that “the scientific method” * that so many pundits still cite and believe in states that a theory is discarded when the evidence goes against it. Here, the mass of evidence against amyloid theory has not broken the grip of the dogmatic knowledge-monopoly. Even as it is acknowledged that tau tangles and not plaques are actually closely associated with loss of neurons, and that plaques were present “10 to 15 years before there are symptoms”, the amyloid theory is still paid obeisance by suggesting that amyloid plays an essential role by “spreading the tau tangles”.
But since plaque pre-dates symptoms by a decade or more, surely it makes more sense to infer that plaque “may be neutral or even beneficial, perhaps attempting to defend neurons that are under attack” since “some amyloid can be found in the brains of most people over 40”.
The New Scientist piece is based on Maruyama et al., “Imaging of Tau Pathology in a Tauopathy Mouse Model and in Alzheimer Patients Compared to Normal Controls”, Neuron, 79  1094-1108; the “et al.” stands for 24 additional names. That article begins, “Hallmark pathologies of Alzheimer’s disease (AD) are extracellular senile plaques consisting of aggregated amyloid β peptide . . . and intraneuronal . . . pathological tau fibrils, while similar tau lesions in neurons and glia are also characteristic of other neurodegenerative disorders” [emphasis added].
Tau tangles, but not amyloid, are known to be associated with a number of neurodegenerative disorders. Where was the need to invoke amyloid rather than tau as a cause of Alzheimer’s in the first place?
Those who question established mainstream dogmas are routinely called “denialists” — “AIDS denialists”, “climate change denialists”, and so forth. In point of fact, it is typically the mainstream thatis truly denialist: evidence denialist. As Max Planck out it long ago, old theories die only as their proponents also pass away; science advances funeral by funeral.
* See Scientific Literacy and Myth of the Scientific Method, University of Illinois Press 1992