An Interview with Greek Cypriot Neuroscientist Dr. Michael Kurnellas

March 8, 2017

By Aria Socratous

Michael Kurnellas is a beautiful mind who keeps the flame of research and innovation at the highest level. His parents are Greek Cypriots and he was born and raised in New Jersey. He received his PhD in Neuroscience from Rutgers University and from 2009 until January 2016 he was a postdoctoral fellow and Research Associate at Stanford University School of Medicine where he focused on the research on multiple sclerosis and on the immunology science of the disease.

He is currently working as a scientist at Alector, an immune-neurology focused biotech start-up advancing first-in-class therapeutics for neuro-degenerative disorders like Alzheimer’s disease, developing therapies that empower the immune system to cure degeneration.

AS: Can you tell us about yourself? Where were you raised and how did you build this beautiful niche for yourself?

MK: Both of my parents are from Cyprus but I was born and raised in New Jersey. I received my Bachelor of Arts in Neuroscience from Drew University, I have a Master of Science in Biomedical Sciences and in 2009 I received my PHD in Neuroscience from Rutgers University I did research on multiple sclerosis at Rutgers and I focused on Neuroscience.

Then I went to Stanford at the end of 2009 to continue the research on multiple sclerosis but also to learn more about the immunology science of the disease. The research was in anti-flammatory amyloid fibrils and the Mechanisms of action of therapeutic amyloidogenic hexapeptides in amelioration of inflammatory brain disease.

AS: Can you talk to us about your discovery concerning the mechanisms of action of therapeutic amyoidogenic hexapeptides in amelioratin of brain disease?

MK: At Stanford, I joined Larry Steinman’s lab to add to my neuroscience background with training in immunology to continue my research on multiple sclerosis. My research was first aimed at investigating the mechanisms of action of small heat shock proteins that are protective in an animal model of multiple sclerosis. With my colleagues, we found that small peptides derived from the protein could form amyloid fibrils and were therapeutic.

When alterations are made to the peptides inhibiting amyloid formation, the peptides were no longer therapeutic. It was very surprising that something that could form an amyloid fibril was protective in an animal model of multiple sclerosis.

Typically, when someone hears the word amyloid, they rightly think of something that is detrimental, such as amyloid beta in Alzheimer’s disease, huntingtin in Huntington’s disease, and alpha-synuclein in Parkinson’s disease just to name a few of many.

We then developed many six amino acid long peptides that form amyloid fibrils, which are likely not forming toxic structures like the larger peptides or proteins. We found that the peptides were anti-inflammatory and can suppress the immune system, thereby reducing the symptoms of the disease in the animal model.

AS: What are you currently working on?

MK: After Stanford, I joined Alector, a biotech start-up that focuses on developing therapeutics targeting the immune system to cure neurodegenerative diseases and cancer. Here I am using my training in neuroscience and immunology to research different targets that play a role in different neurodegenerative diseases, including Alzheimer’s disease and frontotemporal dementia.

AS: What is the difference between Alzheimer’s disease and dementia?

MK: Dementia refers to different diseases that have memory loss and cognitive decline in patients due to damage to cells in the brain. Alzheimer’s disease is the most common type, which is why most people may use the terms interchangeably.

However, patients with other diseases, like frontotemporal dementia, vascular dementia, Creutzfeldt-Jakob disease (“mad cow disease”), Parkinson’s disease, and Huntington’s disease, have dementia, which is caused by mechanisms different than what occurs in Alzheimer’s disease.

AS: Is there research about a complete cure of Alzheimer’s disease?

MK: Yes. There is a lot of interest right now on what causes this disease. There are genetic mutations that increase the risk for the disease, so what I focus on at the company I work at is what are the genetic risks and how do we treat patients that have those risks. We use the immune system to eliminate special aspects of the disease and it seems there is genetic mutation that causes a lot of damage.

We have a very good chance of preventing the disease expand that way. We are trying to find the cure of the disease. A lot of companies put a lot of effort into treating Alzheimer’s disease by developing antibodies against the disease.

There is a lot of work done now trying to cure certain diseases. In Alzheimer’s disease the patient already has the disease, you can not start curing someone until you know that they have it. The patient may suffer already and experience a deficiency in memory and these drugs can reverse that. Dementia can appear to people in early forties. There are genes that play a role in the disease but there are other factors that can affect as well.


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