Alzheimer's Test

Alzheimer’s Disease (AD) is a complex chronic neurodegenerative disease, causing 60-70% of all dementias. Decades of research have identified four prion biomarkers that cause damages in Alzheimer’s patients. Learn about these biomarkers below.

Alzheimer's Prion-Protein Biomarkers:

The following misfolded protein biomarkers are always present in AD patients at all stages:

  • Abeta
  • Tau

The following misfolded protein biomarkers appear in other dementias that can be confused clinically with Alzheimer’s:

  • Synuclein
  • TDP43

Each type of misfolded protein manifests distinct molecular damage to brain cells, playing different roles in different disease stages. The insidious nature of prion proteins has presented immense challenges to detect AD since the disease was first described by its namesake German pathologist Alois Alzheimer’s in 1906.

To thoroughly diagnose the cause of dementia in each patient, we would need to perform biomarker tests on all four misfolded proteins to gain a complete picture of the biomarker profile.  

Learn about the SYNTap-CSF test below, the first FDA Breakthrough Device Designation biomarker test for Parkinson’s, LBD, and other dementias.

What's the SYNTap-CSF Test?

This biomarker test detects misfolded Synuclein aggregates in CSF. It enables doctors to accurately differentiate Alzheimer’s from Lewy Body Dementia (LBD) in all stages of the disease—before the patient shows any Parkinson’s-like motor symptoms.

Accurate diagnosis saves lives! Helping doctors prescribe optimal treatments. Treatment plans can include both drugs as well as lifestyle changes.

Physicians must distinguish between Alzheimer’s vs. Lewy Body Dementia in the early stages to prevent misdiagnosis and incorrect drug treatment.

parkinson's research and care center

Physicians must distinguish between Alzheimer’s vs. Lewy Body Dementia in the early stages to prevent misdiagnosis and incorrect drug treatment.

Why is SYNTap Test Important?

Let’s gain some in-depth understanding of Alzheimer’s and Lewy Body Dementia.

Alzheimer’s and Lewy Body Dementia are two distinct diseases that look very similar in the early stages. 

Alzheimer’s is the primary cause of progressive neurodegenerative dementia, while Lewy Body Dementia represents the second most common cause. 

Alzheimer’s and Lewy Body Dementia take distinct paths of progression and require different treatments. Therefore, it is critical to differentiate between these and reach an accurate diagnosis initially.

Characteristics of Alzheimer's vs. Lewy Body Dementia

At initial presentation, Alzheimer’s patients mainly show a cognitive decline with the particular loss of memory and ability to execute planning. Motor disorders, including Parkinson’s-like symptoms, may also appear at advanced stages of Alzheimer’s disease.

Lewy Body Dementia patients initially show a similar cognitive decline. However, they may also experience visual hallucinations, dizziness, constipation, sleep disorders, and Parkinson’s-like motor symptoms. These symptoms appear earlier in LBD patients compared with Alzheimer’s.

Before the motor symptoms appear, Alzheimer’s and LBD diseases are frequently indistinguishable.

With confusing and mixed symptoms between Alzheimer’s’ and LBD, misdiagnosis frequently occurs, estimated at between 20-50% of all cases. Misdiagnosis leads to mistreatment, which can cause even more harm to patients. 

Alzheimer's and Lewy Body Dementia Treatments

The drugs for Alzheimer’s and Lewy Body Dementia differ considerably. 

For example, drugs that are effective for one disease may cause severe side effects that worsen symptoms in the other. Memantine, a drug commonly used to treat moderate to severe Alzheimer’s, may worsen both cognitive and motor symptoms in LBD patients. Similarly, antipsychotic medications used to treat behavioral disorders in Alzheimer’s patients can cause serious side effects in LBD patients. Finally, when used in Alzheimer’s patients, the LBD medication levodopa has little or no cognitive benefit and may induce or worsen motor disorders.

The proper use of drugs in treating Alzheimer’s and LBD makes accurate diagnosis in the initial stages even more critical. 

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

What Causes Lewy Body Dementia (LBD) And Alzheimer's

LBD results from the proliferation of misfolded Synuclein protein aggregates in the brain. Misfolded Synuclein causes both the cognitive as well as motor symptoms of LBD.

Alzheimer’s patients’ cognitive decline arises from the accumulation of misfolded Abeta and Tau, two additional prion-like proteins in the brain. At advanced stages of Alzheimer’s, patients may also develop Parkinson’s-like motor symptoms. These late-stage symptoms are frequently accompanied by the appearance of misfolded Synuclein or TDP43, another misfolded protein biomarker.

Synuclein is the biomarker key to differentiate Alzheimer’s versus Lewy Body Dementia at the early stages of the disease. 

By using this biomarker test, doctors can accurately diagnose whether the patient has LBD, thereby prescribing appropriate treatment drugs. 

Sign up for the Synuclein Test below.

misfolded protein synuclein

Synuclein is the biomarker key to differentiate Alzheimer’s versus Lewy Body Dementia at the early stages of the disease. 

By using this biomarker test, doctors can accurately diagnose whether the patient has LBD, thereby prescribing appropriate treatment drugs. 

Sign up for the Synuclein Test below.

GET THE SYNTap-CSF TEST

This biomarker test detects misfolded Synuclein, a prion-protein driving such diseases as Alzheimer’s and Lewy Body Dementia (LBD), decades before symptoms. Sign up for email alerts on testing availability.