Maureen Handoko

E-mail: hand0125@umn.edu

Year Entered: 2005

Degrees Received:
B.A., Biochemistry, College of St. Benedict/St. John's University, 2005

Honors and Awards:
Honors, Year 1, Medical School

Thesis Advisor: Karen Hsiao-Ashe, Ph.D., Neuroscience Graduate Program

Thesis Research: 

Alzheimer’s Disease (AD) is a devastating disease currently affecting 26.6 million people worldwide, and its prevalence is predicted to grow fourfold by the year 2050. The disease is primarily characterized by progressive loss of memory function as well as the pathological appearance of β-amyloid plaques and neurofibrillary tangles in the affected brain. Recent research has provided evidence that soluble Aβ oligomers, possibly in conjunction with amyloid plaques, are responsible for eliciting the cognitive impairment associated with the disease. Recently, the Ashe laboratory isolated from a transgenic mouse model of preclinical AD (Tg2576) an Aβ oligomeric species of 56kD (Aβ*56), which impairs memory independent of plaque load or neuronal loss and may contribute to cognitive deficits associated with AD. Our hypothesis is that Aβ*56 initiates cognitive decline in AD and can be employed to predict the development of the disease. Measuring Aβ*56 levels in the cerebrospinal fluid (CSF) might serve as a diagnostic test to identify individuals at high risk for developing AD and allow for early intervention that could prevent or delay the onset of AD. Furthermore, Aβ*56 could serve as a biomarker in primary prevention trials for AD.

My project is currently to develop a capture reagent specific for Aβ*56, using either DNA aptamers or phage display technology to generate antibodies. The capture reagent would eventually be used to develop a sensitive assay to detect Aβ*56 in human CSF samples obtained from longitudinal AD studies or registries.