As we close out our month long discussion on Alzheimer’s, Kineticos’ SVP of Biopharma, Kevin Hampton, leads our expert panelists through a discussion on how dementia and genetics are playing a role in the diagnosis, prevention and treatment of Alzheimer’s disease.


  • Aaron Burstein – SVP of Clinical Development, vTv Therapeutics
  • Sharon Rosenzweig-Lipson – VP of R&D, AgeneBio
  • Jay Mohr – CBO, AZTherapies
  • Jason Kralic – Co-Founder and CEO, Tellus Therapeutics

Kineticos: It was mentioned briefly in one of our previous pieces, should we be screening the general population for dementia?

JM: I certainly think that it’s merited if there’s a family history. It’s something that people should be aware of, perhaps earlier, and the correlation to the use of therapeutic interventions. When there may be earlier evidence of cognitive impairment, you could argue for screening. A much earlier awareness of it proves to be more proactive in therapeutic treatments and other lifestyle changes.

JK: I’m a firm believer that information is power and that with-it families can make decisions on how to care for themselves and prepare for the inevitable challenges of aging. My only concern is how that information is used and any stigma that might occur with it. The information should be owned and controlled by the patient and not used by entities with a commercial or financial interest to make any decisions about them. Otherwise, the focus should be on helping patients and caregivers prepare for their future. Awareness, acceptance, and action on our neurological and mental health is increasing but has a long way to go.

AB: There’s really no option with regard to treatments that could potentially delay the progression, other than participating in a clinical trial. With screening and knowledge, it positions the patients and families to make the decision with the regards to potential trial participation thereby providing them access to possible new therapies.

Kineticos: We’re starting to begin to understand the role genetics play.  How do you think we can minimize the genetic risk factors?

JK: We think about Alzheimer’s as being a constellation of diseases, having a number of causes in which we currently focus on the symptoms and outcomes. As we understand more about the disease, we’re able to consider the patient’s genetic background as it relates to potential efficacy and safety of treatment options. We’re likely to be treating a chronic disease and long-term safety is going to be really important. We’re not going to have the same therapeutic window as cancer drugs. How we approach clinical trial design and eventually treatment decisions is being influenced by understanding our genetic backgrounds and is developing rapidly through the success of products and partnerships e.g., 23andMe. What are we going to do as a pre-MCI patient? What can we do in the decades preceding to put ourselves in a better position from a brain standpoint?  We are influenced by understanding our genetic backgrounds.

SR: It’s important to note that we often have to target something downstream, not directly. We are sometimes looking for where the impairment comes from, thus losing sight of the fact that we may not be able to directly target the impaired gene directly. We have to ensure that when we look for therapeutics, we are using that information wisely and cautiously.

JM: It seems that what we’re learning is a wide range of markers that could be implicated in disease progression, but we don’t know how these evolve and it’s still clearly being worked out. They’re playing a role collectively in disease. This is where oncology has been for a while. It makes sense, given the complexity of the brain, and the various mechanisms associated with Alzheimer’s disease. It is a complex genetic picture. Only with time and large trials collecting all of this information, processing and correlating it to progression of disease outcomes, will we have a better understanding of how all this fits together. It’s a wide-open area for further discussion.

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