Alzheimer's Biomarker Test

Minimal Cognitive Impairment (MCI) is the earliest sign of cognitive decline. Did you know that 1/3 of the people with MCI don’t get Alzheimer’s? That’s magnificent news! The only way to find out for sure is through biomarker testing. 

SYNTap™ Test

What is it?

A biomarker test enabling doctors to accurately differentiate Alzheimer’s Disease (AD) from Lewy Body Dementia (LBD). The biomarker driving LBD is called misfolded Synuclein. 

A test showing negative misfolded Synuclein rules out LBD, but not Alzheimer’s.

In simple terms, it’s like a pregnancy test where the answer is either “yes” or “no.” 👍 👎

What’s the benefit?

Accurate diagnosis saves lives!

misfolded protein synuclein

Accurate diagnosis saves lives!

What do we mean by that? Well, if doctors prescribed a Synuclein-targeted drug to a patient who has no misfolded Synuclein, such treatment could harm instead of help. Biomarker testing empowers doctors to prescribe appropriate medicine that’s just right for YOU. It’s essential to develop holistic treatment plans, integrating drugs, lifestyle changes, and fitness routines for mental and physical health. The earlier, the better! 🕰

Who should take it?

  • If you have previously been diagnosed with Alzheimer’s, the SYNTap biomarker test enables your doctors to identify and differentiate mixed type dementias.

  • If your doctor suspects a neurodegenerative condition, you need this biomarker test to understand what role, if any, misfolded Synuclein plays.

  • If you have suspicions but have not been diagnosed with Alzheimer’s, this test helps your doctor complete a full workup.

How the test works

It’s pretty simple now (after a decade of strenuous development in our lab) 👨‍🔬👩‍🔬 😀

  • Your doctor submits a drop of your cerebrospinal fluid (CSF),

  • We test that sample for misfolded Synuclein,

  • Your doctor gets the result within a week.

Click here to see this simple process illustrated in an infographic.

Why test CSF instead of blood?

CSF testing offers the distinct benefit of reliable, EARLY detection. Why?

Because if misfolded proteins are detectable in blood, this means the notorious troublemakers have breached the blood-brain barrier, spreading throughout the body.
This is far too late! 

The need to differentiate Alzheimer's from LBD

Alzheimer’s and Lewy Body Dementia are two distinct diseases with overlapping symptoms, especially in the early stages. 

The diseases take unique progression paths, therefore requiring different treatments.  Differentiating them matters greatly. 

It’s like this. Long road trips often require moving from one freeway to another. If you miss that pivotal connecting point and drive down the wrong road, you’ll waste a lot of precious time and fuel to get back on track, not to mention the I-told-you-so’s from your significant other. 😖 🛣 🚙

Challenges to early-distinguish Alzheimer's vs. LBD

Let’s continue the road-trip metaphor. The beginning of the journey looks similar in every way. As you drive closer to the destination, things start to change, subtly at first, then suddenly.

Imagine it’s 1990, the Berlin Wall is about to come down. You take this historic drive from West Germany towards East Germany. As you cross the border, the smooth well-maintained road instantly populates with potholes. The colors transform from vibrant to dull: people’s clothing, the buildings, the foliage, even the air smells different. And it all happened so abruptly. 

This is similar to the disease journey of Alzheimer’s and LBD. Here are some key points:

  • Initially, Alzheimer’s patients mainly show a cognitive decline such as loss of memory and executive functions. For advanced Alzheimer’s patients, motor symptoms may also appear.

  • Similarly, LBD patients first show comparable cognitive decline. They may also experience visual/olfactory hallucinations, dizziness, constipation, sleep disorders, etc.

  • Like Alzheimer’s, advanced LBD patients may also show motor symptoms, a hallmark of Parkinson’s.

  • In both Alzheimer’s and LBD, the shared symptoms are strikingly similar before the noticeable movement symptoms start. 🤷🏻‍♂️

These mixed symptoms make Alzheimer’s and LBD nearly impossible for doctors to early-distinguish using traditional methods.

Harmful consequences of misdiagnosis

Brain diseases are notoriously difficult to track and treat due to the nasty characteristics of misfolded proteins (aka prions). Misidentifying prions results in detrimental treatment side effects.

Simply put, Alzheimer’s drugs may harm LBD patients and vice versa. Here are three examples:

  • Memantine, a drug commonly used to treat moderate to severe Alzheimer’s, may worsen both cognitive and motor symptoms in LBD patients.

  • Antipsychotic medications used to treat behavioral disorders in Alzheimer’s patients can cause serious side effects in LBD patients.

  • Levodopa, an LBD medication, has little or no cognitive benefit when given to Alzheimer’s patients and may even induce or worsen motor disorders.

Prescribing proper drugs for the right disease makes precise early-stage diagnosis even more critical. 

Because with the wrong drugs, the patient suffers more harmful consequences. 

As Dr. Seuss eloquently wrote in Fox In Socks: Moose juice is not good for gooses. And goose juice is not for mooses. 🤓

Comparing Alzheimer's and LBD biomarkers

This section is for people who ate protein (eggs with the yolks, anyone? 🍳) for breakfast today; therefore, their super-charged brain is prepped for the science-y stuff.  

  • LBD results from the proliferation of misfolded Synuclein protein aggregates in the brain. (See, told ya!) Misfolded Synuclein causes both cognitive and motor symptoms in LBD patients.

  • In Alzheimer’s, cognitive decline arises from the accumulation of two types of misfolded brain proteins: Abeta and Tau.

  • In advanced Alzheimer’s, patients may also develop Parkinson’s-like motor symptoms.

  • These late-stage Alzheimer’s symptoms are associated with misfolded Synuclein or TDP43, another misfolded protein biomarker.

So in neurodegenerative disorders, four biomarkers drive disease progression: Misfolded forms of Synuclein, Abeta, Tau, and TDP43. 

Did you know brain diseases are often misdiagnosed? 
Conservatively estimated up to 50%! Let’s END that.

parkinson's research and care center

Did you know brain diseases are often misdiagnosed? 
Conservatively estimated up to 50%! Let’s END that.

Biomarkers driving Alzheimer's

For the brave souls determined to finish the rest of this page, we recommend extra eggs tomorrow morning to renourish your brain cells (also helps biceps). 🥚💪

The following misfolded protein biomarkers are always present in Alzheimer’s patients at all stages:

  • Abeta
  • Tau

Furthermore, two other misfolded protein biomarkers appear in advanced Alzheimer’s patients: 

  • Synuclein
  • TDP43

Each misfolded protein type causes distinct damage to brain cells. The insidious nature of prions makes Alzheimer’s diagnosis immensely challenging. It has been this way since Dr. Alois Alzheimer first described the condition in 1906.

Therefore, to completely diagnose what’s driving Alzheimer’s, all four biomarker tests are required.   

Don’t forget your extra eggs in the morning. All you egg-heads, have you tried them 5-minute soft-boiled? 😜 🤓

GET THE SYNTap™ TEST

This biomarker test traces misfolded Synuclein, a prion-protein present in many brain diseases. And detects it decades before symptoms!!!  Sign up for email alerts on testing availability. 📋 🔬

Share this great news with someone you love! 💖

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