• DISCERN™ is the only extremely accurate test for identifying and distinguishing AD from other forms of dementia.
  • DISCERN™ requires only a tiny skin sample, taken like a regular blood draw at the doctor’s office.
  • The test is relatively inexpensive, and far less expensive and intrusive than any existing tests for diagnosing AD, which include invasive spinal punctures (CSF Biomarkers) and PET scans.
  • Each biomarker has been proven, in human clinical trials conducted at major universities to be extremely accurate, with a sensitivity and specificity greater than 95% in both detecting AD and differentiating AD from other dementias.

How It Works

The DISCERN™ test requires only a small skin sample (simple punch biopsy) obtained at your healthcare provider’s office.  The specimen is then shipped to our laboratory for testing.

The skin sample is incubated for a few weeks and grown to threshold volumes of greater than 1,000,000 cells, after which it is subjected to various assay measurements for 3 separate proprietary biomarkers, each of which, independently, identifies and differentiates AD from other dementias.

The three biomarkers comprise an AD-Index assay, a Morphometric Imaging assay and a PKC Epsilon assay. The test can determine the level of synaptic loss in the brain before the onset of amyloid plaques or tangles and is accurate even in the earliest stages of the onset of AD (i.e., years 1-4).


The 3 Biomarkers

The Science

The 3 biomarkers were developed after many years of research at the Blanchette Rockefeller Neuroscience Institute by a team of scientists led by Dr. Daniel Alkon, the Director of the Institute, who previously had spent 30 years conducting research in neuroscience and memory at The U.S. National Institutes of Health (NIH) as a Medical Director in the National Institute of Neurological Disorders and Stroke (NINDS) and as Chief of the Laboratory of Adaptive Systems. Confirmation of the biomarkers accuracy consisted of double blinded clinical trials conducted at major universities, where age matched controls, non-Alzheimer’s Disease dementia patients and AD patients had skin samples taken and then subjected to the biomarker tests. The biomarker test results were hyper-validated by subsequent brain autopsies of the suspected AD patients, and the use of confirmed non-AD dementia patients in the trials (e.g., Huntington’s Diseases, Parkinson’s or other confirmed forms of dementia), which confirmed that all 3 biomarkers were extremely accurate.

AD-Index Biomarker
A small specimen of skin fibroblasts is incubated to an 80-90% confluence stage. An inflammatory agonist (a small nano-peptide that induces Erk1 and Erk2 phosphorylation in fibroblasts) stimulates the skin specimen. Quantitative imaging of the phosphorylated Erk1 and Erk2 is then used to identify and differentiate Alzheimer’s Disease (AD) from Non-AD dementia (Non-ADD) and Age-matched control (AC) specimens.

More detail here: AD Index biomarker

Morphometric Imaging Assay Biomarker
The cultured skin specimen is stimulated with an extracellular matrix composed of an array of macromolecules, forming networks which are dysregulated in AD skin fibroblasts. Networks are rapidly formed for Age-matched control and non-AD dementia cells, but not for AD cells. The rate and extent of network formation can be quantified and is a highly accurate diagnostic biomarker of AD that corresponds to autopsy-demonstrated pathologic hallmarks of AD – amyloid plaques and neurofibrillary tangles. Biochemical determinants of network formation are similar in many respects to synapse network formation among culture neurons.
This biomarker accurately diagnosed AD patients and distinguishes them from AC specimens and Non-ADD dementia specimens.

More detail here: Morphometric biomarker

PKCε Biomarker
Protein Kinase C ε (PKCε) is primarily expressed in the brain and is known to be associated with AD pathophysiology. For this biomarker, PKCε-specific antibodies are used with the cultured skin specimen to quantify relative levels of PKCε and to distinguish AD patients from non-ADD and AC patients. AD patients demonstrate a comparative deficit in PKCε and a different response to the ab stimulus when compared to AC and Non-ADD. These differences were found to correspond closely in the AD patients to the presence of amyloid plaques and neurofibrillary tangles.

More detail here: PKCe biomarker

Learn More:

Disclaimer: This test was developed and its performance characteristics were determined by the Rockefeller Neuroscience Institute and NeuroDiagnostics LLC. It has not been cleared or approved by the US Food and Drug Administration. The FDA does not require this test to go through premarket FDA review. It should not be regarded as investigational or for research. This test should be interpreted in context with other clinical findings. The NeuroDiagnostics’ laboratory is certified under the Clinical Laboratory Improvement Amendments (CLIA) as qualified to perform high complexity clinical laboratory testing. Although these tests are highly accurate, rare diagnostic errors may occur. Possible diagnostic errors include sample mix-up, erroneous specimen identification, technical errors and clerical errors. The report from NeuroDiagnostics does not represent medical advice. Any questions, suggestions, or concerns regarding interpretation of results should be forwarded to a physician skilled in interpretation of the relevant medical literature.