CSF-Specific APOE Glycoforms as Biomarkers for Alzheimer’s Disease Progression
Categories: “Neurological Disorders” “Diagnostics“
Reference #: 2017-037
OTC Contact: Ruchika Nijhara, Ph.D., MBA, CLP (Directory Information | Send a Message)
A method of detecting a cerebrospinal fluid-specific (CSF specific) glycoform of Apolioprotein E (APOE) in a subject’s CSF or plasma sample, in order to diagnose Alzheimer’s disease risk and progression.
A glycoform of APOE is an isoform of APOE that differs with respect to the number or type of glycans attached to APOE. With the present invention, one or more CSF-specific glycoforms can be detected in a sample from a subject’s plasma or CSF. A difference between the level of the CSF-specific forms of APOE from the sample as compared to a control level of CSF-specific APOE from the subject or population of subjects, which do not have Alzheimer’s disease or a risk of Alzheimer’s disease greater than the risk of Alzheimer’s disease in the general population will lead to conclusive diagnoses by investigators.
- Determining the progression of Alzheimer’s disease or an increase in the risk of developing Alzheimer’
s disease in a subject
- Can determine the efficacy of a selected treatment for slowing the progression or delaying thedevelopment of Alzheimer’s disease in a subject
- Can be combined with other tests such as brain imaging, neurological exams, blood tests etc. to determine Alzheimer’s disease progression.
Stage of Development
Georgetown investigators suggest that measures of particular modified versions of APOE may correlate with pathogenic processes of Alzheimer’s disease and may be useful as modifiable biomarkers of Alzheimer’s disease or Alzheimer’s disease risk. They previously published that the levels of modified forms of APOE differs in post-mortem samples of the brains of APOE4 Alzheimer’s disease patients compared to APOE3 Alzheimer’s patients.
Rebeck GW, Reiter JS, Strickland DS, Hyman BT, 1993, "Apolipoprotein E in sporadic Alzheimer’s
disease: allelic variation and receptor interactions," Neuron, 11: 575-580.
Martin-Rehrmann MD, Hoe HS, Capuani EM, Rebeck GW, 2005, "Association of apolipoprotein J-
positive -amlyoid plaques with dystrophic neurites in Alzheimer’s disease brain," Neurotox Res, 7:231-242.
Zhou Y, Zhao W, Al-Muhtasib N, Rebeck GW, 2015, "APOE Genotype Alters Immunoglobulin Subtypes in Knock-In Mice," J Alzheimers Dis 46(2):365-74.
DiBattista AM, Stevens BW, Rebeck GW, Green AE, 2014, "Two Alzheimer’s disease risk genes increase entorhinal cortex volume in young adults," Front Human Neurosci 8:779.