I’m excited to share with you all my first interview for My OT Spot with Isaac Bishof. Isaac is a PhD candidate at Emory University in Atlanta, Georgia, and his focus is on Alzheimer’s disease research.
Isaac is studying how a group of proteins influence Alzheimer’s disease. He and his team are looking at the molecular mechanism of Alzheimer’s disease and how certain proteins may play a role in its progression.
I jumped at the chance to interview him since many Occupational Therapists work with Alzheimer’s disease but may not know the back-story of the disease. I want to give him a big “Thank you!” for taking the time to sit down with me.
You study Alzheimer’s disease for your Doctoral research. Can you give us a synopsis of what Alzheimer’s disease actually is?
Alzheimer’s disease (“AD”) is a neuro-degenerative disease and is most commonly associated with memory loss and dementia in older individuals. Dementia is a “catch all” term for a decline in mental ability severe enough to interfere with daily life, but doesn’t necessarily mean it’s caused by Alzheimer’s disease. Memory loss is just one component of AD-linked dementia; there are many other mental capabilities being compromised by the disease.
The brain has several regions each with specialized jobs or functions. While Alzheimer’s disease affects all parts of the brain, the effects are particularly strong in the hippocampus and frontal cortex.
The hippocampus is the region of the brain most responsible for memory formation and memory retrieval. The loss of hippocampal functions leads to the memory problems commonly associated with the disease. The frontal cortex, which is responsible for personality, complex problem solving, and planning is also affected by AD.
Alzheimer’s disease is the most common cause of dementia at this time. It is not part of “normal” or healthy aging, although age is the largest risk factor. Chances of developing AD doubles every five years after age 65, and by age 85 the risk is 50%.
Currently there are no methods to effectively prevent, treat, or cure Alzheimer’s disease. The drugs available only moderately treat symptoms and do not stop disease progression.
Do you think we’ll find a cure for Alzheimer’s disease in our lifetime?
I do think in our lifetime researchers will find a way to treat Alzheimer’s disease by slowing the progression, and maybe finding preventative measures for it. I don’t think we’ll actually cure it.
I think we can find a way to slow the disease’s progress by 3-4 years, which would delay the dementia symptoms. “Curing” AD would be very difficult since neurons in the patient’s brain have already died.
In order to cure it, we would have to create something that allows the brain to grow new neurons, which currently isn’t possible. Our best efforts will be focused on managing the disease by finding the best ways to slow its progression and improving preventative measures.
What are you currently studying for your research?
With our research, we’re looking to understand the biomechanical mechanism of Alzheimer’s disease. Our group’s research is diverse, but I am specifically looking at how the aggregation of RNA binding proteins may lead to disease progression.
The splicing protein called U1-70K aggregates in Alzheimer’s Disease. The aggregation is thought to disrupt U1-70K’s role in RNA processing. This disruption may contribute to neural death, and neuronal death is what leads to the disease. My team discovered that these groups of RNA proteins aggregate in Alzheimer’s disease. So now our research is trying to figure out why.
Do we know what actually causes Alzheimer’s Disease?
We aren’t yet entirely sure what the exact cause of Alzheimer’s disease is. It’s currently is believed that the build-up of proteins (such as amyloid plaques) in the brain play a central role in disease progression. It is the loss of neurons through these build-ups that lead to symptoms of dementia in AD.
Neurons are responsible for relaying the information to and within the brain. Hence, they are crucial for all types of brain functions ranging from breathing to complex thought. The destruction of these neurons leads to the loss of short term memory, decreased problem solving skills, and personality changes.
How is an individual diagnosed with Alzheimer’s disease?
Right now, the Alzheimer’s diagnosis still isn’t 100% clear until after death where an autopsy of the brain is performed. An autopsy usually isn’t performed unless the patient is in a research trial; most facilities do not have the resources for an autopsy.
Doctors can diagnose probable AD while living if the patient meets these three criteria: dementia, neurofibrillary tangles, and amyloid plaques. If the patient meets this criteria, they can be diagnosed with AD according to our current medical definition.
Are there any promising current medical options available for Alzheimer’s?
There are medications available that work to inhibit acetylcholinesterase, the enzyme which inactivates acetylcholine (ACh) at the synapse. Inhibiting this enzyme prevents the normal breakdown of ACh and is a way of compensating for the lowered concentrations of ACh characteristic of Alzheimer’s disease.
In my opinion, these medications really only temporarily slow the worsening of symptoms. The medications are basically like giving caffeine to an exhausted person, they will still need to sleep to sleep eventually so the exhaustion is not “cured.”
I don’t think the current medications are really that effective, but I do think researchers will find a more effective treatment and better drugs for the disease in our lifetime.
What do you see happening with Alzheimer’s research in the next 5-10 years?
There are a currently a lot of projects looking at genes and RNA. Scientists are going to have a lot more data than we have now. This could illuminate new pathways that are important in disease pathogenesis that might lead to better drug targets than we what we have now.
We also might have a blood or spinal fluid biomarker test to administer to patients to diagnose the disease while the patient is still living. This would be huge for drug research as well, since a major barrier to AD drug research is that it’s very hard to get a cohort where every participant truly has AD.
Is there anything else currently going on with research in the field that you’re excited about?
I’ve seen something interesting with drug trials working to monitor amyloid-beta plaque levels, and all of them failed. This sounds bad, but it allows us to look at new things since the last 20 years we’ve focused on primarily amyloid-beta plaques and their role in AD.
A lot of evidence shows that removing the plaques doesn’t seem to help people, so it allows us to put research toward other new branches of productive research.
Okay, last question: Do you believe it’s true that “keeping the mind active” lowers the risk of developing Alzheimer’s disease?
Studies do show that individuals that have completed higher levels of education, like Master’s/Doctorate level degrees, are less likely to develop AD and may delay its development. People who keep their brains more active might have more plasticity to deal with the death of neurons as they age. We aren’t really sure why but higher education does tend to “stave off the disease” in studies.
For more on this theory, check out this article from the University of Madison-Wisconsin.
This doesn’t mean that someone with six degrees is 100% safe from getting the disease, though. They just have lower odds based on current research. Even so, I don’t think it hurts to keep your brain active throughout your lifespan to potentially lower your risk.
After talking with Isaac, it really made me realize what a challenging problem Alzheimer’s disease will be to solve. While it sounds like there still is a long way to go, it’s reassuring to know there are such brilliant minds working on it.
I have a much greater appreciation for what scientists are doing every day when it comes to better understanding this complex and devastating disease.
I want to again thank Isaac for putting up with my barrage of questions and for keeping the really “science-y” stuff simple enough for a non-PhD student to comprehend :).
I learned way more about Alzheimer’s disease than I thought I ever would, and I hope you all found this interview as informative as I did. I really look forward to keeping up with the latest research and trends toward better treatments and preventative measures.
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