Forgetting where you put your keys or your phone, blanking on someone’s name, or struggling to remember a specific word are all normal occurrences that can happen at any age. But they are also events that occur more frequently and naturally as we get older. The aging process results in structural changes to our brains, just as it does for the rest of our bodies. Beginning in our early 30s, our memory performance declines, as do our abilities to multitask, learn new things, and come up with novel solutions to problems. The result is that the same tasks get subtly but progressively harder and require more neural engagement.

That process, often referred to as “normal” cognitive aging, is gradual and linear. Normal cognitive aging also leaves some performance mostly intact, including overall vocabulary, memories for events from previous years or decades, the ability to focus on single tasks, and the skill to mobilize known solutions to familiar problems. These declines are observable in cognitive performance tests and are often distressing and annoying, but they do not usually restrict day-to-day functioning.

In contrast, disordered aging—such as Alzheimer’s disease, vascular or Lewy-body dementia, or other aging-associated diseases like Parkinson’s—can come on suddenly, progress rapidly, and affect nearly all areas of cognitive performance. These diseases, particularly if untreated, trend toward profound decline in overall memory and cognitive functioning, resulting in loss of independence and the eventual death of affected individuals.

The good news is that the past two decades have brought significant breakthroughs in understanding the dynamics behind both normal and disordered cognitive aging. Moreover, many neurochemical events, such as declines in acetylcholine, dopamine, GABA, and other neurotransmitters, appear to be shared across normal and disordered presentations. Thus, better understanding one form may also help us treat others. Over time, it is plausible that many more cases of both normal and disordered cognitive aging will become preventable or even reversible.

As average lifespans continue to increase, understanding the causes—and treatments—of cognitive aging becomes ever more urgent. Therefore, it should be no surprise that this work has long been a major focus of several Michigan Psychology labs.

One line of inquiry, led by Dr. Thad Polk, looks at neural dedifferentiation: the aging brain’s tendency to become less selective about which brain areas are activated as we complete specific tasks. For example, older people tend to show more neural activation across multiple brain regions when identifying faces or places, whereas younger people complete the same tasks with more selective and efficient use of specific areas. Polk and others have linked this process to declining levels of the inhibitory neurotransmitter GABA, raising the possibility of targeted interventions, though considerably more research is needed before they can be developed.

For over 20 years, Dr. Patricia Reuter-Lorenz’s lab has focused on another age-related shift in brain patterns: As we get older, we increasingly draw on both the left and right hemispheres to perform tasks that could have been completed with more engagement of just one hemisphere earlier in life. Based on those observations, Reuter-Lorenz pioneered the CRUNCH hypothesis, which argues that this bilateral recruitment compensates for other age-related declines in processing power (such as the neural dedifferentiation described above). Reuter-Lorenz has shown that cognitive training can help partially reverse this pattern and enables people to complete more difficult tasks while relying less on brain architecture to compensate. Along with the late Dr. Denise Park, Reuter-Lorenz advanced the influential Scaffolding Theory of Aging and Cognition, asserting that later-life cognition is shaped by cumulative life experiences. According to Scaffolding Theory, activities like exercise and lifelong learning can help improve the brain’s ability to compensate for age-related declines, whereas conditions like cardiovascular disease and chronic stress can worsen it.

Another cognitive neuroscientist, Dr. Cindy Lustig, has research focused on both normal cognitive aging and on changes seen in Parkinson’s disease. In her normal cognitive aging research, she investigates differences in performance between younger and older groups, including the intriguing finding that the same situational conditions (such as the risk of losing money) can motivate one group to perform better, but the other to perform worse, on the same tasks. In her Parkinson’s work, she focuses on how declines in neurotransmitters, particularly acetylcholine, appear to be connected to reduced performance in attention, memory, and motivation. Because the same neurotransmitter declines are also seen in other forms of aging, this work has important implications even beyond improving Parkinson’s treatments.

But cognitive aging outcomes are also strongly influenced by a variety of health and social determinants. Risk factors such as cardiovascular disease and depression can substantially worsen the effects. Other factors, such as maintaining a large, active social network, can substantially improve them. Understanding these influences is extremely important because they are often modifiable at both community and individual levels.

For example, Dr. Laura Zahodne and her lab focus on social contributors to dementia risk, including size of social networks and the availability of resources within neighborhoods and other communities. Importantly, Zahodne’s work also examines disparities among racial, ethnic, and socioeconomic groups, with many minority groups having substantially higher risk of dementia due to reduced availability of resources. Real-world interventions based on this research can reduce disparities between groups and meaningfully delay or prevent the onset of dementia for many people.

Finally, Dr. Toni Antonucci has spent much of her career studying how the social environment affects aging across the lifespan. A pioneer of the Convoy Model of Social Relations, which views relationships as falling within metaphorical “circles” of closeness (e.g., spouses and best friends, extended family and friends, coworkers and casual acquaintances), Antonucci adapts her work to real-world interventions. Recent threads in her work have examined the impact serving as a caregiver can have on cognition, as well as the disparate impact of the COVID-19 pandemic on cognition across populations.

Taken together, this pioneering research from Michigan Psychology faculty offers real hope that cognitive aging may not always be inevitable or permanent.

Read on for more details about each lab’s research.

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Thad Polk - Computational & Cognitive Neuroscience Lab

Many older adults notice that thinking gets a little harder with age: It takes longer to figure out a new phone, to recall a name, to juggle several things at once. My lab studies why, by using technologies like functional magnetic resonance imaging (fMRI).

When a young adult sees a face, one pattern of brain activity lights up; when they see a building, a clearly different one does. In many older adults, those different patterns start to blur together. We call this neural dedifferentiation, and it isn't confined to vision; we find the same blurring in the brain regions that handle hearing and movement. And this matters for everyday life: older adults with sharper, more distinct brain patterns do better on tests of processing speed, reasoning, and mental flexibility, while vocabulary and accumulated knowledge, which tend to hold up well with age, are unrelated.

We think part of the explanation is chemical. GABA, the brain's main inhibitory neurotransmitter, is what lets neurons quiet their neighbors so that one representation can stand out from another. We use the same MRI scanner to measure brain chemistry, and we've found that GABA levels fall with age, including within the same people tracked over years. What’s more, older adults with more GABA in a given brain region have crisper signals there.

Perhaps the most encouraging finding is how much people differ. Some brains hold their sharpness far better than others, and that is exactly the kind of variation that eventually makes interventions possible. Our current work follows people as they age for up to fifteen years, asking who declines, when it begins, and why. We are also planning to add blood-based Alzheimer's markers, to see if those same mechanisms are at work in the disease.

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Patricia Reuter-Lorenz - Cognitive & Affective Neuropsychology Lab   

Just over 25 years ago, the Reuter-Lorenz Lab was among the first to document that healthy older adults (ages 65-80) use both sides of their brain while performing certain cognitive tasks, whereas younger adults show more lateralized, asymmetric brain activity. Specifically, older people show activity in both the left and right cerebral hemispheres during verbal and spatial short-term memory tasks. By contrast, younger adults accomplish the same tasks with more lateralized engagement of the left hemisphere for verbal tasks and the right hemisphere for spatial tasks. We also demonstrated that bilateral activity was associated with optimal task performance for older adults: The more bilateral the brain activity, the better the performance. The interpretation we offer is that older adults recruit additional neural circuitry to compensate for other age-related neurocognitive changes when achieving the same level of performance as younger adults.

We expanded on that idea by advancing the framework known as “compensation related utilization of neural circuits hypothesis,” or CRUNCH. According to CRUNCH, as task difficulty increases, the brain engages more circuitry across both hemispheres to meet demands. This pattern of increasing bilaterality is observed in both older and younger adults as tasks get more difficult. However, older adults reach a threshold or crunch point to recruit broader neural circuitry for easier tasks compared to younger adults. Once the crunch point is reached, task performance and neural activity decline. More recently our team demonstrated that cognitive training can help to reverse the CRUNCH pattern: Using brain imaging, we showed that multiple days of short-term memory training helped both older and younger adults improve performance while decreasing reliance on additional compensatory circuitry.

In addition to CRUNCH, my late colleague Denise Park and I advanced the widely influential Scaffolding Theory of Aging and Cognition. According to the Scaffolding Theory, the status of an individual’s cognition and the rate of their decline in later life are jointly due to the lifelong influence of enriching and depleting influences, many of which are modifiable. Positive lifestyle choices like exercise and performing cognitively engaging activities help build scaffolds against declining performance, while factors like cardiovascular risks or chronic stress can reduce the brain’s ability to compensate.

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Cindy Lustig – Cognition & Aging Lab

Research with young and older adults in our lab examines age differences in attention, memory, and motivation. We are interested in understanding the factors that can impair or improve performance in each group. For example, conditions under which people lose money for mistakes lead to better performance for young adults, but the same conditions can actually reduce performance for older adults. We are trying to understand whether this is because losing money for mistakes increases older adults’ attention to their mistakes, if it reduces their motivation, or some combination of the two. On the other hand, we often find that older adults are more motivated to perform well and are better at maintaining their engagement with a task, and that in some cases this can lead them to perform even better than young adults do.

In another set of studies, we examine how the neurotransmitters associated with attention, memory, and motivation change with age-related diseases like Parkinson’s disease. By examining how those changes affect people’s cognition, we can identify risks for falls, which might help people modify their environments to prevent them. Our work has also been used to help identify and test new drug treatments in clinical trials. Some of the underlying mechanisms of Parkinson’s, such as declines in neurotransmitters like dopamine and acetylcholine, also occur to lesser degrees with other forms of cognitive aging. Therefore, it is plausible that learning how to better treat Parkinson’s may also help us learn to address other aging-related processes.

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Zahodne Lab – Michigan Cognitive Aging Project

A series of landmark Lancet Commission reviews report that 45% of dementia cases can be attributed to specific preventable causes, such as physical inactivity, cardiometabolic disease, vision and hearing loss, and depression. My lab seeks to uncover additional risk and protective factors for dementia that individuals and/or communities can act on. For example, we have shown that having a larger social network and living in a neighborhood with more resources (regardless of your own personal resources) are each associated with better cognitive aging. My lab also works to clarify neural mechanisms underlying these effects. While some protective factors prevent pathology from accumulating in the brain (“brain maintenance”), others appear to help the brain continue to function well despite the accumulation of pathology (“cognitive reserve”).

In response to the high and increasing number of older adults at risk of dementia, our work reveals multiple complementary avenues for delaying or even preventing clinical symptoms. For example, our research points to more frequent interaction with friends as the “active ingredient” in social networks for maintaining cognitive health. In addition to guiding more specific recommendations for individual behaviors, our work can also inform stakeholders about neighborhood-level interventions that could have even broader impacts than individual-level interventions. Indeed, an important goal of our work is to identify modifiable social and structural factors underlying health disparities across racial groups.

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Toni Antonucci – Life Course Development Program

Work in our lab focuses on social relations and health (physical/psychological/cognitive functioning) across the life span. Recently, our work has involved several concrete empirical strands. One line examines caregiving's toll on cognition, with a 2025 study assessing both cross-sectional and longitudinal associations between caregiving, caregiving stress, and caregivers' own cognitive functioning. A related strand of research examines health inequities during the pandemic, offering a snapshot of ethnic disparities in physical, mental, and cognitive health across metro Detroit during COVID-19. I have also performed extensive research on the relationship between technology and social ties, including authoring a late-2025 study on diversity in how older adults use information and communication technology to stay connected with their social networks.

My work has also examined cross-national and economic dimensions and disparities in aging. A 2026 study compared gender differences in work expectations and psychological distress among Baby Boomers in the United States and South Korea. Another project turned to domestic economic inequality, examining twenty-year trends in physical, mental, and functional well-being by household income level, with a focus on the "forgotten" lower-middle class who fall outside most need-based social safety nets.

Factors such as chronic stress significantly worsen cognitive aging outcomes, while factors such as the presence of a large, active social network significantly improve them. Together, these projects show my Convoy Model of Social Relations framework being applied to increasingly specific, policy-relevant populations — caregivers, ethnic minorities, cross-national retirees, and economically squeezed households — that can help reduce the negative effects of cognitive aging across populations.