ParkinZheimer℠

Decades of prion research led us to a new paradigm — Brain diseases exist on a spectrum called ParkinZheimer. Discover how this philosophy empowers breakthroughs. 

Amprion recently received FDA Breakthrough Device Designation for detecting misfolded Synuclein. This prion biomarker drives Alzheimer’s, Parkinson’s Disease (PD), Lewy Body Dementia (LBD), and other brain diseases.

We diligently apply this prion detection science to identify other biomarkers for ParkinZheimer diseases. Accurate early detection fast-tracks drug development.

Let’s dive in for a more in-depth look.   

The ParkinZheimer viewpoint

Old school thinking

For three decades, researchers and scientists have pursued cures for Alzheimer’s and Parkinson’s. In spite of hefty spending of $100+ billion dollars globally, we’ve come up EMPTY.

And yet, the need to find cures for ParkinZheimer diseases has never been greater.

featured image - test for Alzheimers

And yet, the need to find cures for ParkinZheimer diseases has never been greater.

Consider these grim facts:

  • More than 8 million Americans currently suffer from Alzheimer’s, Parkinson’s, and LBD combined.

  • There are more than 1.2 million new cases diagnosed each year.

  • By 2050, brain disease victims will grow to nearly 25 million in the US alone!

  • By that time, cost of care for these diseases will exceed $1.3 Trillion!!!  

Historically, Alzheimer’s and PD drug research was conducted in separate silos as two distinct diseases. These walled-garden studies isolated findings and excluded knowledge sharing. Consequently, this approach stifled progress and snuffed out breakthroughs.

The new outlook

Instead of turtle-plodding advancements, Amprion is racing to a cure. Our detection science empowers drug R&D through biomarker tracking. What do we mean by that?

The goal is to speed drug development. To make it happen, effective clinical trials are key. We enable pharmaceutical companies to select patient-participants based on their biomarker profile. That’s a mind-blowing big deal!

When drugs are tested this way, we will get real answers. Every insight will boost our Big Brain Data nexus.   

Ultimately, we’ll discover cures through cross-pollinating from all sides of the brain health aisle. 

clinical trials

Ultimately, we’ll discover cures through cross-pollinating from all sides of the brain health aisle. 

Why do we think the ParkinZheimer paradigm is essential in our race to cure brain diseases? Let’s take a closer look at how these diseases have been dealt with traditionally.

Alzheimer's & PD are distinct disciplines

For more than 100 years, Alzheimer’s and Parkinson’s have been viewed as two completely different, unrelated diseases. For example:

  • Alzheimer’s and PD patients visit different doctors in separate buildings on the same campus.

  • Neuroscientists and clinicians are encouraged to focus their careers exclusively on one of the diseases.

  • Research funding for Alzheimer’s generally excludes Parkinson’s and vice versa.

    • The National Institutes of Health (NIH) funds research for these diseases from completely different institutes.

    • Alzheimer’s is funded through the National Institute on Aging (NIA) and Parkinson’s through the National Institute of Neurological Disorders and Stroke (NINDS).

According to a government website, at the time of this writing, there are currently:

  • 2,574 clinical trials in various stages for Alzheimer’s
  • 2,891 clinical trials in various stages for Parkinson’s

Do Alzheimer's and PD share similarities?

Molecular science advancements have uncovered new prion biomarkers, enabling us to track various neurological diseases accurately.

Our prion research has led us to understand how Alzheimer’s and Parkinson’s share surprisingly similar traits:

  • Late-stage PD often progresses to severe dementia, closely resembling Alzheimer’s.

  • Misfolded Synuclein is found in both Alzheimer’s and PD patients, 40% and 95%, respectively.

Conclusion

Contrary to centuries-old thinking, ParkinZheimer diseases are not caused by aging. Instead, they appear to be present either at birth or early adulthood.

Once the protein misfolding process is triggered, the asymptomatic stage begins. The disease progresses undetected for decades, causing irreversible damage to the brain. By the time symptoms appear, it’s TOO LATE!   

The traditional viewpoint has governed the way we analyze these diseases and produced no breakthroughs!

It's time for a change.

Let's unite and race together to a cure!

shared focus on science

ParkinZheimer Frequently Asked Questions

We consider Alzheimer's and Parkinson's exist on a spectrum called ParkinZheimer. These two diseases overlap, resulting in irreversible cognitive, motor, and autonomic dysfunction. The spectrum also includes Amyotrophic Lateral Sclerosis (ALS), FrontoTemporal Dementia (FTD), Progressive Supranuclear Palsy (PSP), and Multiple System Atrophy (MSA). While originally described as distinct diseases, they share common underlying elements.

Both Alzheimer's and Parkinson's are now believed to result from the destruction of brain pathways caused by prion proliferation. The prions involved include misfolded Abeta, Tau, and Synuclein. These prions cause irreversible cell death, spreading from cell to cell through established connections. Almost all cases of Alzheimer's contain Tau prions, but up to 40% may also contain Synuclein prions. Conversely, almost all Parkinson's cases contain Synuclein prions, but Tau prions appear to be present in a significant percentage as well. While Parkinson's initially presents as a motor disease and Alzheimer's presents as a cognitive disease, these differences may blur as both diseases progress. At Amprion, we consider all brain diseases exist on a spectrum called ParkinZheimer™.

ParkinZheimer diseases share a common prion origin. So far, we don't know the cause of how prions come into existence. The three major prions (or misfolded proteins) affecting ParkinZheimer patients are Abeta, Tau, and Synuclein. Every ParkinZheimer patient has a unique combination of prions in various regions of the brain. This unique biomarker profile, plus its location in the brain, determine the symptoms and progression.

Examples of ParkinZheimer include Parkinson's, Alzheimer's, Lewy Body Dementia, Parkinson's Disease Dementia, Frontotemporal Dementia, Pick's Disease, Progressive Supranuclear Palsy, and Corticobasal Degeneration.

Currently, ParkinZheimer diseases are diagnosed by brain imaging. There is considerable overlap in clinical presentation among the disorders. Imaging works best at more advanced stages. As a result, early diagnosis is extremely challenging. Doctors often modify their diagnosis as symptoms change and the disease progresses. New biomarker tests involving the detection of prions, such as misfolded Abeta, Tau, and Synuclein, will revolutionize early diagnosis. These biomarker tests are performed using cerebral spinal fluid, blood, and other tissue biopsies.

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