Alzheimer’s research should set its sights on prevention

There has been an Alzheimer’s disease paradox for the past 20 years.

The search for the cause of this disorder has been carried out under a very limited spotlight that has produced no clear benefits for patients at risk of this dementia or for those already diagnosed with it.

It is time we go in a different direction.

The trackless clinical progress is all the more baffling when you consider the more than 100,000 clinical and scientific papers published on the subject of Alzheimer’s during the past 20 years.

A considerable amount of the Alzheimer’s research done during this period has attempted to validate that Alzheimer’s is caused by the excessive accumulation of a sticky substance in the brain, called “Abeta” for short.

Although several versions of the “Abeta hypothesis” have been put forward, its main thesis is that Abeta is responsible for the neurodegeneration and cognitive loss seen in people with the disease.

This dogmatic view has spawned more than 40,000 papers dealing mainly with the biochemistry, genetics, pathology, molecular activity and clinical effects of Abeta.

The Abeta hypothesis has so influenced and dominated Alzheimer’s research that many clinical workers and researchers regard it as the gold standard of scientific investigation.

But, despite the monumental bibliography that Abeta research has generated, patients today are no better off, medically speaking, than when the disease was described by Alois Alzheimer in 1907.

The Abeta hypothesis has been put to the test in a series of pharmaceutical-sponsored clinical trials using anti-Abeta drugs in order to reduce aggregation or clear it completely from the brain.

But despite the virtual clearance of Abeta from the brain or limiting its aggregation, none of the anti-Abeta medications used was able to improve cognitive function or slow the neurodegenerative progress characteristics of Alzheimer’s.

In fact, some of the treated patients developed adverse reactions to the anti-Abeta treatments, the most serious being brain swelling.

News articles estimate that Big Pharma has pumped more than $1 billion into these failed clinical trials and continues to test other “me-too” drugs, hoping for a different outcome.

Common sense dictates that limiting research to a single theory weakens our confidence that good science is being practiced.

Prevention, rather than finding a dubious nostrum for Alzheimer’s, is a more realistic strategy, knowing what is known about the pathology of the disease.

Prevention should aim at preserving normal cognitive function in people for as long as possible.

The best time to apply preventive measures is during middle age, aiming at asymptomatic or mildly symptomatic individuals when early interventions can be most effective.

Mounting evidence indicates that Alzheimer’s is a disorder evolving mainly in elderly people who show preventable vascular risk factors.

These risk factors are reported to progressively lower cerebral blood flow in the brain.

When blood flow to the brain drops to a critical level, mild cognitive difficulties and later Alzheimer’s can flourish.

Vascular risk factors such as cardiovascular disorders, hypertension and high cholesterol, among others, can be treated early with clinical follow-ups for long-term changes.

And neuroimaging tools that can identify low blood flow to the brain prior to the onset of mild-moderate cognitive difficulties can lead to interventions that can be immediately applied to patients, thus lowering their risk of developing Alzheimer’s.

This story was originally published August 24, 2016 at 6:29 PM with the headline "Alzheimer’s research should set its sights on prevention."