As a way to highlight World Alzheimer’s Month this September, six researchers at Gladstone talk about their work and how it can help us better understand the disease. They also discuss some of the biggest challenges on the horizon, and share how research can eventually lead to better treatments for Alzheimer’s disease.
I'm interested in studying the interaction between neurons and the immune cells that reside in the brain known as microglia.
A substantial portion of Alzheimer’s disease patients experience silent seizures—or bursts of abnormal neuronal activity—that are associated with faster cognitive decline. My research shows that in a mouse model of Alzheimer’s disease, microglia aid in suppressing silent seizures. But certain genetic mutations might impair their function and lead to worsening of silent seizures.
We are trying to help identify therapeutic interventions that can disrupt this cycle and hopefully slow, prevent, or reverse cognitive deficits.
My team and I hypothesize that in Alzheimer's disease, neurons and microglia engage in a vicious cycle of abnormal activities, which may promote cognitive decline. We are trying to help identify therapeutic interventions that can disrupt this cycle and hopefully slow, prevent, or reverse cognitive deficits.
I study the effects of a particular protein related to Alzheimer’s disease: apoE. A certain version of this protein can significantly increase your odds of developing the disease. In the lab, I use CRISPR-Cas9 technology to create disease-related mutations in human stem cells grown in culture dishes. Then, I turn these cells into neurons to see how they’re affected by the mutations, and whether they exhibit Alzheimer’s-like traits.
One of the biggest challenges I see right now in the field of Alzheimer’s disease is specifying patient populations.
One of the biggest challenges I see right now in the field of Alzheimer’s disease is specifying patient populations. It’s an incredibly complex disease, and many really smart people working on genetics are trying to parse out different subpopulations of Alzheimer’s patients. I think therapies targeted toward specific populations are more likely to be successful.
Our lab studies apoE4, the greatest genetic risk factor for Alzheimer’s disease. Having even one copy of apoE4 increases your chance of getting the disease by three times.
ApoE4 has many different effects on different cell types, including neurons. Studying how apoE4 causes neuron loss and memory deficits can give us concrete molecular targets to start Alzheimer’s drug development.
Studying how apoE4 causes neuron loss and memory deficits can give us concrete molecular targets to start Alzheimer’s drug development.
I study energy metabolism in neurons, with the goal of better understanding how metabolism is altered in neurodegenerative diseases like Alzheimer’s disease.
Alzheimer’s disease is the most common cause of dementia worldwide, and it remains unclear how metabolism and genetic risk factors combine and contribute to the disease.
Alzheimer’s disease is the most common cause of dementia worldwide, and it remains unclear how metabolism and genetic risk factors combine and contribute to the disease. With our work, we can begin to understand ways of boosting energy metabolism in susceptible neurons, and ultimately help develop novel therapeutic approaches for treating Alzheimer’s disease.
Emerging evidence has shown that disruption of the blood-brain barrier and deposits of a blood clotting protein in the brain are not merely consequences of the progression of Alzheimer’s disease. Instead, they play a critical role in causing immune activation and neurodegeneration.
Our goal is to provide a better understanding of the molecular and cellular triggers of neurodegeneration.
To study the role of blood-brain barrier disruption in the disease, we developed cutting-edge tools that allow us to monitor the different types of brain cells and their interactions in live mice. Our goal is to provide a better understanding of the molecular and cellular triggers of neurodegeneration.
I believe this will help us find novel therapeutic interventions for Alzheimer’s disease.
I chose to study Alzheimer’s disease because my grandpa suffered from this disease, and I saw first-hand how difficult it can be for the patients, the caregivers, and the families. Being the first in my family to pursue a PhD, I hope to contribute to finding a cure for this debilitating disease through research.
Being the first in my family to pursue a PhD, I hope to contribute to finding a cure for this debilitating disease through research.
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Gladstone researchers show that ApoE4 from neurons plays a much more critical role in the disease than previously thoughtNews Release Research (Publication) Alzheimer’s Disease Center for Translational Advancement Neurological Disease Huang Lab
Gladstone discoveries compete head-to-head with other scientific advancementsAwards COVID-19 Traumatic Brain Injury Alzheimer’s Disease Huang Lab Paz Lab Weinberger Lab Chaturvedi