Study declaring Alzheimer's to be a "brain disease" proven to be fabricated

The battle against Alzheimer’s has recently taken a controversial turn. Long-held theories about its cause are being challenged, which is sparking heated debates.

Now, emerging research points to the possibility that Alzheimer’s is actually an immune system disorder.

Critical data possibly fabricated

Recently, the Alzheimer’s research field witnessed a shockwave. A 2006 research article, published in the acclaimed journal Nature, has received renewed scrutiny.

The paper had presented the beta-amyloid protein subtype as the Alzheimer’s instigator.

However, recent revelations in the journal Science suggest that this potentially game-changing data might have been fabricated.

In June 2021, the FDA approved aducanumab, a drug designed to target beta-amyloid. This decision added to the controversy because the supporting evidence for its effectiveness was incomplete and inconsistent.

While some physicians insist it’s premature to deem it fit for use, others argue in favor of giving it a fair shot.

This begs the question: why are millions still hanging in the balance, waiting for a successful Alzheimer’s cure?

Preventing beta-amyloid accumulation

Over the years, the scientific gaze has been fixed on beta-amyloid, the elusive protein implicated in the onset of Alzheimer’s disease.

The primary focus has been on preventing the harmful accumulation of this protein in the brain.

Unfortunately, this intense fascination hasn’t exactly been fruitful. In fact, with their laser focus on the beta-amyloid protein, scientists may have ignored other viable and potentially enlightening avenues.

Understanding beta-amyloid

Beta-amyloid is a protein that naturally occurs in the brain, and plays a role in helping nerve cells communicate. Think of it as a messenger that helps keep your brain functioning smoothly.

However, problems arise when beta-amyloid starts to accumulate and clump together, forming sticky plaques between nerve cells.

These plaques can interfere with how brain cells communicate, leading to issues with memory and thinking.

Most scientists believe that when too much beta-amyloid forms these plaques, it triggers a chain reaction that damages and eventually kills brain cells.

This is why, in recent decades, researchers have been so focused on finding ways to reduce beta-amyloid levels in the brain; they were hoping to slow down or even prevent the progression of Alzheimer’s.

Immune system intruder

Researchers at the Krembil Brain Institute, part of the University Health Network in Toronto, have been studying Alzheimer’s disease for over three decades. Their findings offer a fresh and surprising perspective on the condition.

“We no longer think of Alzheimer’s as primarily a disease of the brain. Rather, we believe that Alzheimer’s is principally a disorder of the immune system within the brain,” explained Donald Weaver, professor of chemistry at University Health Network.

Alzheimer’s and the brain’s immune system

The immune system, present in every organ, consists of cells and molecules that repair injuries and fight infections.

This holds true for the brain’s immune system too. It’s always ready to repair injury or tackle invading bacteria – but here’s where trouble brews.

Researchers at the Krembil Brain Institute suggest that beta-amyloid, often blamed for causing Alzheimer’s, may not be harmful on its own.

Instead, they believe it plays a crucial role in the brain’s immune system, helping to protect against threats.

However, while it may be necessary for defense, its actions can sometimes backfire, leading to unintended harm.

The new theory suggests that beta-amyloid finds itself in a bind. Due to striking similarities between bacterial membranes and brain cell membranes, it can’t distinguish between friend and foe.

In its bid to protect, beta-amyloid ends up attacking the very brain cells it should be safeguarding.

This misdirected assault leads to progressive brain cell function loss and culminates in dementia. It’s a tale of the immune system playing the villain by failing to differentiate between the enemy and the ally.

Alzheimer’s: An autoimmune disorder?

Given this perspective, Alzheimer’s disease can be seen under the umbrella of autoimmune diseases where the body ends up attacking itself.

Although traditional autoimmune therapies might not work for Alzheimer’s, the researchers are hopeful.

They believe that focusing on other immune-regulating pathways within the brain could lead to effective treatment approaches.

This isn’t the end of the story though. Several equally intriguing theories are beginning to surface.

Some researchers classify Alzheimer’s as a mitochondrial disease, while others attribute the condition to a particular brain infection or abnormal handling of metals within the brain.

A shift in perspective

With over 50 million people worldwide affected by dementia, fresh perspectives and innovative ideas have never been more crucial.

Alzheimer’s isn’t just a health crisis. It’s a ticking socioeconomic time bomb that demands a better understanding of its causes – including its possible links to the immune system – and effective treatments.

Scientific data and breakthroughs, although valuable, should not overshadow the human aspect of the disease.

The focus should also remain on improving the quality of life for Alzheimer’s patients, easing their challenges, and offering emotional and practical help.

It is imperative that research serves the people it is intending to help, and keeps their needs and experiences at the forefront.

The study is published in the journal Science.

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