Alzheimer’s disease is not only an emotionally taxing condition — it can also wreck a person financially.

The Economic Cost of Dementia in Australia 2016-2056 report reveals that Alzheimer’s disease, along with other dementias, have cost Australians $14.25 billion in 2016. This translates to an average cost of a whopping $35,550 per patient.

While there are plenty of technological advancements focus on improving the life quality of patients, some companies continue to pursue permanent solutions to the incurable, progressive disease.

On July 5, Eisai Co., Ltd., and Biogen Inc. unveiled the detailed phase 2 results of an experimental drug called “BAN2401.” It turns out that the promising medication slowed down the progression of Alzheimer’s by 30 percent.

There are currently 425,000 people in Australia with Dementia, a number that’s expected to top a million by 2056.

“Dementia Australia welcomes all research into Alzheimer’s disease and dementia to improve the lives of the 425,000 Australians currently living with dementia.” Says Kaele Stokes, Executive Director Consumer Engagement, Policy and Research.

Worldwide, Alzheimer’s disease is an even bigger problem — affecting nearly 50 million people in 2017 and potentially costing nations a grand total of US$1 trillion in 2018.

Despite these figures, patients with Alzheimer’s disease are still left with no reliable treatment — except for medications that alleviate the disease’s symptoms, such as depression, disorientation, anxiety, and sleep disorders.

That’s why the entire Alzheimer’s community, including medical practitioners, researchers, and patients, are met with a new wave of optimism with the new Alzheimer’s drug.

Companies Eisai and Biogen disclosed more information about their phase 2 results at the Alzheimer’s Association International Conference.

Millions of people have Alzheimer’s disease and right now it’s a death sentence,” said Keith Fargo — director for scientific programs at the Alzheimer’s Association. “So any time  we see positive results from a trial that appears to show disease modification, that gives us hope — but it’s a cautious hope.

How the New Drug Works

It’s no secret that Alzheimer’s is a complex disease.

The scientific community’s best explanation for the disease thus far is the amyloid hypothesis, which points to the accumulation of extracellular beta-amyloid proteins in the brain as the primary influence behind the disease’s progression.

When amyloid proteins are misprocessed, they begin to form “plaques” outside the nerve cells — causing tissue death and brain shrinkage.

Once this process is set into motion, the person may start to experience the early, telltale signs of Alzheimer’s disease.

In simple terms, the drug purportedly functions as the humanized version of a mouse antibody that specifically binds with these beta-amyloid plaques. Its action involves the neutralization and elimination of the toxic, soluble build-ups — protecting nearby cells from damage.

This is the first late-stage anti-amyloid antibody study to successfully achieve statistically significant results at 18 months, said Eisai chief clinical officer and chief medical officer Lynn Kramer, M.D.

The drug was originally developed by the company, BioArctic Neuroscience, and licensed to Eisai. The latter then was granted exclusive rights to conduct further research and manufacture the new drug.

Summary of Phase 2 Study Findings

Topline results of the final analysis for the drug indicate a significant reduction in amyloid plaques after 18 months of treatment. The study involved 856 patients with early-stage Alzheimer’s who underwent five different dose regimens:

  • 2.5 mg/kg, twice a week
  • 5 mg/kg, once a month
  • 5 mg/kg, twice a week
  • 10 mg/kg, once a month
  • 10 mg/kg, twice a week

The benefits are notably more prominent in patients who were receiving the highest treatment dose.

The 18-month results of the BAN2401 trial are impressive and provide important support for the amyloid hypothesis,” said Jeff Cummings, M.D., of Cleveland Clinic Lou Ruvo Center for Brain Health. “I look forward to seeing the full data set shared with the broader Alzheimer’s community as we advance against this devastating case.

How Does It Work?

The new Alzheimer’s drug reduces the formation of amyloid plaques and protects nerve cells from deterioration. It wasn’t observed to stop amyloid plaque build-up altogether, but the phase 2 findings prove that the new drug is indeed potent in slowing down Alzheimer’s disease.  

The theory is if we can interrupt the plaque formation, and these toxic forms of amyloid, hopefully, we can interrupt that whole process and slow down memory loss,said neurology professor Stephen Salloway at Brown University and director of neurology at Butler Hospital in Providence, Rhode Island. “That’s why we’re excited about this finding.

Throughout phase 2, the Alzheimer’s drug was observed to have a good tolerability profile. This bodes well for patients and investors who can spearhead the market adoption of the drug.

If eventually made market-ready, the drug will become the first-ever treatment for patients in the early stages of Alzheimer’s disease — unlike the plethora of expensive medications available today that only target the disease’s symptoms.

Looking Beyond Beta-Amyloids

Apart from beta-amyloids, the progression of Alzheimer’s disease is also attributed to two other things: Tau proteins and microglia.

Tau proteins are known to form neurofibrillary tangles inside nerve cells. Their production, however, is triggered via an immune response to the accumulation of amyloid plaques.

In other words, tau proteins come into the picture after amyloid proteins begin to be misprocessed and aggregated.

Microglia, on the other hand, are the immune cells of the human body’s central nervous system.

Their main function is to eliminate pathogens and waste cells in the event of infection or injury.

However, a study shows that microglia can damage synapses along with amyloid plaques. This consequently accelerates neurodegeneration and worsens related disorders, like Parkinson’s disease, ischemic stroke, and Alzheimer’s disease.

Since the Alzheimer’s drug addresses the problem of excessive beta-amyloid build-up, it should also theoretically hinder the presence of tau proteins and microglia in the brain.

We think this result is really the first of its kind,” said Kramer. “Robust enough to approach regulatory authorities to discuss next steps.

Since Dementia, a type of Alzheimer’s, affecting seventy percent of cases, is the second leading cause of death among Australians (according to Dementia Australia), the final analysis for the new Alzheimer’s drug shows great promise to those suffering from the disease.

Moving Forward

To the Alzheimer’s community, the phase 2 findings for the new drug can be seen as a resounding success. The question is, can the drug pass a phase 3 clinical study and obtain FDA approval?

A phase 3 study will introduce a larger group of authorities to facilitate and validate the effectiveness of the drug. Patients may not be able to see BAN2401 products in pharmacies soon, but they have every reason to be optimistic given the recent advances this 2018.

What are your thoughts on this potential Alzheimer’s drug? Could it be the first actual treatment for Alzheimer’s disease?

Leave a comment below and join in the discussion.