Two neuropathologic features observed in the brain of patients with Alzheimer disease (AD) dementia are the presence of plaques composed of beta-amyloid (Abeta) peptides and intracellular neurofibrillary tangles containing hyperphosphorylated Tau (tubulin-associated unit) proteins. These 2 groups of molecules are the most established biomarkers of the disease used in clinical and research practice. Positron emission tomography (PET) imaging using US Food and Drug Administration approved amyloid radiotracer (amyloid-PET) to visualize the presence of amyloid lesions in the cerebral cortex is available in some specialized centres. Measuring Abeta42 peptides and certain phosphorylated Tau (such as p-Tau181) proteins in cerebrospinal fluid (CSF) may be used as a means to assess the presence of amyloid pathology. In particular, the use of the p-Tau181/Abeta42 ratio has been shown to be an excellent surrogate marker of amyloid plaque burden, caused by increased deposition of beta-amyloid 1-42 in the brain.
These assays should not be used to predict the development of dementia or other neurologic conditions or to monitor response to therapies. They are for assessment of adults with cognitive impairment being evaluated for Alzheimer disease and other causes of cognitive impairment.
A positive cerebrospinal fluid (CSF) beta-amyloid 42 (Abeta42), total Tau (t-Tau), or phosphorylated Tau (p-Tau181) result, or p-Tau181/Abeta42 ratio does not establish a diagnosis of Alzheimer disease (AD) or other cognitive disorder. These results should be interpreted in combination with other clinical diagnostic and radiologic evaluations.
Failure to adhere to the specimen collection instructions provided may result in falsely low Abeta42 concentrations and potential misdiagnosis of AD.
Specialist Biochemistry
SENB
3 weeks