Researchers race to detect Alzheimer's sooner using $3.9M grant

Nov 15, 2024

3 min

Chris Martens


Too often, people learn they have Alzheimer’s disease when it’s too late. The changes in the brain that lead to the disease manifesting with symptoms have already been occurring for decades.


Researchers at the University of Delaware will attempt to detect the disease sooner through a new study that examines changes in the arteries and brain tissue in midlife adults in their 50s and 60s. The findings of this work, funded by a nearly $4 million grant from the National Institute on Aging (NIA), could identify the earliest mechanisms linking vascular aging to the loss of brain tissue integrity, leading to new targets for interventions aimed at preventing age-related cognitive impairment.


“People who develop high blood pressure or stiffening of the aorta and carotid arteries in midlife are at a much higher risk for developing cognitive impairment or dementia in late life,” said Christopher Martens, the principal investigator of the study.


Martens, an associate professor of kinesiology and applied physiology in UD's College of Health Sciences and director of the Delaware Center for Cognitive Aging (DECCAR), is working closely with Curtis Johnson, an associate professor of biomedical engineering in the College of Engineering and leader of the neuroimaging biomarker core within DECCAR, on research funded by a nearly $4 million grant from the National Institute on Aging (NIA), a division of the National Institutes of Health (NIH).


“A lot happens as we age, so we’re aiming to pinpoint the timing and exact mechanisms that cause these changes in midlife adults,” Martens said.


This latest grant extends DECCAR’s ongoing Delaware Longitudinal Study for Alzheimer’s Prevention (DeLSAP), which seeks to study how risk and protective factors for dementia are related and change over time. Those eligible for DeLSAP could also meet the criteria for participating in the new study.


In his Neurovascular Aging Laboratory, Martens studies mechanisms leading to the stiffening of arteries, while Johnson is specifically interested in measuring the stiffness of the brain.


“As a person ages, the brain gets softer and breaks down, and we’re looking to see whether changes in arterial stiffness and patterns of blood flow in the brain cause this decline,” Johnson said.


Changes in blood flow to the brain come from controllable factors. Smoking, cardiovascular health, diet and exercise all impact blood flow positively and negatively.


“A lot of aging research is done at the end of life,” Johnson said. “We want to look at midlife and try to predict what happens later in life so we can prevent it.”


While the brain gets softer with age, arteries get stiffer.


“We hypothesize that midlife increases in stiffness in blood vessels cause damaging pulsatile pressure to enter the brain,” Martens said. “We believe this is one of the reasons we start to develop cognitive issues at an older age because the brain is exposed to increased pressure; that pressure is likely inflicting damage on surrounding brain tissue.”


In Johnson’s Mechanical Neuroimaging Lab, researchers will use high-resolution magnetic resonance elastography (MRE) to determine where brain damage occurs and what specific brain structures may be affected.


“From an MRI perspective, most researchers look at AD and other neurodegenerative diseases like multiple sclerosis with an emphasis on detection in a hospital setting,” Johnson said. “Using highly specialized techniques we’ve developed, we focus on the earlier side and how these changes progress into disease from the neuroscience side, emphasizing prevention.”


Together, they’ll seek to learn whether arterial stiffness causes the kind of cognitive impairment seen in AD or whether the decline is associated with a loss in the integrity of brain tissue.


“If we can prove arterial stiffness is playing a causal role in cognitive aging, that would provide further support for focusing on blood vessel health as an intervention for delaying AD or other forms of dementia versus solely focusing on the brain,” Martens said.

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Chris Martens

Chris Martens

Associate Professor, Kinesiology & Applied Physiology

Prof. Martens's laboratory is interested in understanding mechanisms by which impaired vascular function contributes to cognitive declines.

Alzheimer's DiseaseAgingClinical TrialsCerebral Blood FlowVascular Aging
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The similarities in the two datasets brought us to the realization that fault sections without large magnitude earthquakes control the overall occurrence of big events on transform faults. When we had that observation in 2008, that might have been a one-off, but getting back this new data and seeing such similar behavior was a new insight into what's happening in the fault. How does that tell you about how earthquakes occur on land? Warren: On land, people spend a lot of time looking at how rainwater and groundwater move in a fault system, and how that influences the behavior of the fault. In the oceans, we have an unlimited amount of water. Once the rock cracks, the water is going to get in there. Being able to look at how a fault changes through the earthquake cycle — which we've now measured most of on this one fault — can help us understand what is universal about how faults work, and how rock friction works. And one of the big players is water. That's why the rock samples that my lab works on matter. Fault structure is another thing that we've been trying to understand. We know from on land that some parts of a fault are linear, while other parts have lots of strands and maybe contain more fractures and that, if you start putting water in the picture, this can limit or change how water moves into the system. Now, we have these very high-resolution maps of the seafloor, where we can see, for the first time, where the fault itself is. One of the next things we want to understand is how fluid gets into the fault, and then how friction in a fault changes when water is there. Why is this important? Warren: The next step is to translate the understanding that we've gained from this specific fault to understanding how faults behave in general. This is the longer path to really understanding earthquake hazards. It's not going to change our hazard models tomorrow, but hopefully it will in the decades to come. To reach Warren directly and arrange an interview, visit her profile and click on the "contact" button. Interested reporters can also email MediaRelations@udel.edu.

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