-Short Biography

Ellen started her study bio engineering in 2005 at the Free University of Brussels (VUB). After finishing the bachelor in 2008, she chose for the profile medical biotechnology in her master, focusing on biochemistry and biophysics. She did an internship at Janssen Pharmaceutica NV, optimizing different screening tests for tracing hard metals in new pharmaceutical ingredients. After a master’s thesis on the characterization of a tRNA modification enzyme complex she decided to stay in the protein field and started a PhD on a topic related to Alzheimer’s disease. More specific, she is investigating the link between Apolipoprotein E (ApoE) and the amyloid beta peptide. She will do her research part time at VUB and part time at UTwente. In her free time she gives dance courses, plays tennis and loves to travel.

-Contact Information -

Ellen Hubin (MSc, ir)


University of Twente

Institute for Biomedical Technology

and Technical Medicine MIRA

Zuidhorst ZH155

Drienerlolaan 5

7522 NB  Enschede, the Netherlands

PO-box 217

7500AE Enschede, the Netherlands

P +31-(0)53-489-XXXX

F +31-(0)53-489-1150


-Own Research in NBP-

TOPIC: ApoE genetic variation as causative factor in Alzheimer’s disease

Amyloid beta peptide (Aβ) is a compound in the brain which has been linked to the development of Alzheimer’s disease (AD). The Aβ peptide is produced by cleavage from the Amyloid Precursor Protein (APP) by sequential action of β- and γ-secretases. AD patients sometimes show a higher overall Aβ production. The level of Aβ in the brain is normally tightly regulated by a balanced production (γ-secretase pathway) and degradation mechanism (by insulin-degrading enzyme, neprilysin, matrix metalloproteases). The Aβ degradation machinerie in AD patients is however less functional and a reduction in the activity of several Aβ-degrading enzymes has been seen.

During the last decade, it became apparent that soluble rather than deposited Aβ is associated with AD. Among the constituents of soluble Aβ, small oligomeric forms were increasingly associated with neuropathology. There is now evidence that Aβ oligomers do not affect neuronal viability in general, but interfere specifically with synaptic function. Loss of meaningful synaptic function in the brain of AD patients shatters their capacity to encode and retrieve memories.

It is not clear how the Aβ peptide can cause AD and it is thought that Aβ might not be solely responsible for the onset of the disease. One major risk factor for AD involves the cholesterol carrying protein Apolipoprotein E (ApoE). This multifunctional circulating lipoprotein consisting of 299 amino acids exists as three different isoforms: ApoE2, ApoE3, and ApoE4, which differ in primary sequence at one or two residues. Patients with AD are significantly more often homogeneous ApoE4 allele carriers compared to controls and thereby the ApoE isoform represents the most important and single genetic risk factor for AD determined today. The identity of the interplay between Aβ and ApoE4 is studied but not clear, but ApoE and Aβ are both found in the pathological lesions in the brain characteristic for AD. The ApoE2 isoform on the other hand was found to decrease the risk for AD.

This study will ensue to describe in detail the mechanism by which the specific ApoE isoform can affect the lifecycle of Aβ by employing a multidisciplinary approach. These disciplines include cell biology, neurobiology, biophysics and nanotechnology. Potential targets of the Aβ-ApoE link with AD which have been suggested in literature, but have been left unexplored to-date, will be identified. The aims of this project are:


To investigate the effect of the different ApoE isoforms on the cleavage of Aβ from its precursor protein APP.


To investigate how the different isoforms of ApoE affect the formation of toxic oligomerisation intermediates of Aβ.


To investigate how the presence of the different ApoE isoforms affects clearance of Aβ by a number of known degradation mechanisms.

Publications of interest

(Means publications that either describe your work or your own)


J. Kim, JM. Basak and DM. Holtzman. The role of Apolipoprotein E in Alzheimer’s disease, Neuron 63 (2009), 287-303.