Show Notes

Read the study from the University of California, San Francisco (UCSF), “Traumatic Brain Injury Strikes 1 in 8 Older Americans,” mentioned by Dr. Chin at 0:30 on the UCSF website.

Learn more about Dr. He’s study in the article, “TBI linked to long-term cognitive decline in preclinical Alzheimer’s disease,” published on Healio’s website.

Learn more about the Cognitive-Communication in Aging and Neurogenic Disorders Laboratory (CCANDL) on their lab website.

Learn more about Dr. He on the CCANDL website.

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Transcript

Intro: I’m Dr. Nathaniel Chin, and you’re listening to Dementia Matters, a podcast about Alzheimer’s disease. Dementia Matters is a production of the Wisconsin Alzheimer’s Disease Research Center. Our goal is to educate listeners on the latest news in Alzheimer’s disease research and caregiver strategies. Thanks for joining us.

Dr. Nathaniel Chin: Welcome back to Dementia Matters. According to a 2024 study from the University of California, San Francisco, roughly one in eight older adults in the United States are diagnosed with and affected by traumatic brain injury, also known as TBI. Typically a result of falls, crashes or being struck by something, these injuries can impact both short-term and long-term brain function. How exactly do they impact cognitive decline? Joining us today to discuss the connections between TBI and cognition is Dr. Deling He, a postdoctoral research associate at UW’s Cognitive Communication in Aging and Neurogenic Disorders Laboratory known as CCANDL. In 2025, Dr. He and researchers from CCANDL conducted a study investigating how traumatic brain injury is associated with cognitive speech changes linked to Alzheimer’s disease before presenting these results at the 2025 Alzheimer’s Association International Conference, where you did make a lot of news, Deling. Welcome to Dementia Matters. I’m very excited to have you. We’ve given a brief definition in the intro for TBI, but can you define what TBI is a bit more for our listeners?

Dr. Deling He: Yes. Thank you very much for having me here on Dementia Matters. TBI or traumatic brain injury usually refers to the damage to the brain caused by an external force like a fall, a blow to the head or a car accident or sports collision. It can lead to temporary symptoms like confusion or disorientation or more lasting effects such as memory problems or long-term cognitive decline or changes in behavior.

Chin: That’s a great full definition. Thank you. Now I’m wondering though, especially when you mentioned sports, how is TBI different from having a concussion?

He: Yes, that’s a really great question. I think TBI is more like an umbrella term. Concussion is a type of TBI. It is generally considered a mild TBI. The brain has been jostling, causing a temporary disruption in function, but often without major structural damage in the brain that can be seen in standard imaging like an MRI. TBI is the broader term that includes everything from a mild concussion to more severe injuries involving bruising, bleeding or long-term damage to the brain.

Chin: You mentioned something that really caught my attention. That was the structural changes that we can actually capture on imaging. Do you have to have structural images–or structural change, I should say–captured on an image in order to have TBI? I think of TIA and how that’s different than a stroke is that in stroke, we actually see the evidence on an MRI, whereas in a TIA, we just don’t see it. I’m just wondering, like, is that a part of the criteria for TBI?

He: I don’t think it’s part of the criteria for TBI, which means it’s not always the case that you can observe the structural changes in the brain. That’s usually the severe TBI if you can observe structural changes, but for mild TBI like a concussion or just a fall, sometimes you cannot find the direct evidence from the neuroimaging.

Chin: That makes a lot of sense because I’ll see a lot of patients who clearly had more than a concussion, traumatic brain injury, and it was years ago, but when we look at their MRI it looks totally normal. We don’t actually see that. I know that MRIs–we’re as good as our tools and it’s not perfect, but we don’t see it. I guess that fits what I see in the clinic too. I’m also wondering then, what are the most common ways people incur a TBI? We mentioned some generic things like falls and crashes, but is that the most common?

He: Yes, definitely. Falls are the leading causes, especially in young children and older adults. Car accidents, sports injuries like American football, soccer and hockey, those are very common for sports collision. Combat-related injuries in veterans are also common sources for TBI.

Chin: Oh wow, okay. With all that context, now I’m going to go back to a question I always like to ask, which is why did you decide to study TBI and then study TBI in the context of Alzheimer’s disease?

He: This study actually was initially led by Olivia Goulette, who is an excellent master’s student and graduated earlier in the spring from our lab. Together with Dr. Kim Mueller, my mentor, I also mentored Olivia on this project since I joined the lab. The reason why we want to study TBI in the context of Alzheimer’s is because we are fascinated by the connection. Both TBI and Alzheimer’s are known causes for dementia and they may have more links than we once thought. We now know that the long-term effects of TBI can lead to brain changes that look very similar to the hallmarks of Alzheimer’s disease. Specifically, it’s the accumulation of amyloid beta and tau in the brain. This leads to our key research question–if a person already has these early Alzheimer’s pathological changes in the brain, does a history of TBI act as an additional hit, making their decline in cognition and language faster or worse? That’s what we set out to explore in the study.

Chin: That’s a great question. That’s why I’m looking forward to going over your results. But before we do, because I think a lot of our listeners, I’m sure they’ve heard of TBI or traumatic brain injury, but we also hear a lot more about CTE or chronic traumatic encephalopathy. How are those things different from Alzheimer’s disease? Because they are separate processes.

He: Yes, that’s a really good question. The simplest way to think about it is the cause. TBI is caused by an external force to the head and it’s an event. On the other hand, Alzheimer’s is a progressive disease that develops from changes in the brain over time. While both can lead to dementia and involve the buildup of proteins like tau, how and where they are built up is different. In Alzheimer’s, we know those proteins accumulate in a very specific pattern, typically starting from memory centers. In contrast, the long-term effects of TBI, sometimes known as CTE, chronic traumatic encephalopathy, involve a different pattern, especially the tau pathology. The tau often clusters around the brain’s small blood vessels and in the deeper areas of the brain’s cells. This is really uncommon for brains that are without repetitive brain trauma. This can also lead to different symptoms like impulsivity and mood swings. They also sometimes appear earlier in life than typical Alzheimer’s disease. In short, they have different causes and different brain patterns and often have different symptoms, even though they can have a lot of overlap in symptoms and in protein accumulation.

Chin: That was a great explanation. I’m not going to lie, I was a little bit nervous about it because I recently was at a community event and someone asked me this and I gave a similar answer. Yours is better, but I wasn’t incorrect. One of the things I want to confirm, because I want to make sure that I go forward with the right information, because I absolutely understand the symptoms can overlap. They can be different, too, but they can overlap. Then the protein part, that’s where I was getting at. Both conditions, traumatic brain injuries, CTE and Alzheimer’s can have the tau protein, that tauopathy. It’s a slightly different tau is my understanding, but it’s tau there. But only Alzheimer’s would have the amyloid. Am I right in saying that? Would someone with CTE or traumatic brain injury also have elevated amyloid because of that? Or would that just be co-pathology where both processes are happening?

He: I think that there are a lot of controversial findings regarding the amyloid accumulation in the brain. Some studies find there is accelerated or increased amyloid accumulation following TBI, but some don’t. There is a very recent study that found that it’s not necessarily the global accumulation or the global cortical accumulation of amyloid that is increased after TBI, but more like the pattern of amyloid in the brain is different. They kind of find that following TBI, there is more amyloid and tau-related accumulation in the frontal and parietal regions in the brain, which is usually seen later in Alzheimer’s changes. In Alzheimer’s disease, frontal and parietal accumulation occurs later in the disease progression, but they can find this very early if followed by a TBI history.

Chin: See, that’s fascinating. I’m glad we kind of touched on the controversy within the field. We don’t know fully yet, so it’s still being explored. That is very interesting and the importance of biology and studying this with our biomarker tests and for our participants to come in so that we can study this over time. All right, so now getting back to your study, what exactly did you find now that we know what you were looking for?

He: Yes, so prior research has established that individuals with preclinical Alzheimer’s pathology, which means they aren’t yet showing noticeable cognitive symptoms but the brain changes related to Alzheimer’s already occur, those people experience faster declines in their language ability. Our study extended these findings by showing that a history of TBI can further worsen their language abilities. This effect is detectable even 28 to 36 years after the brain trauma. Specifically, we saw that these individuals with a prior TBI showed a faster decline in their speech fluency. They spoke more slowly, they used fewer words and had more pauses and repetitions in their speech. This suggests that a past head injury may specifically weaken the brain’s language network, making them more vulnerable to the effects of Alzheimer’s pathology.

Chin: Wow, that’s incredible. We do actually see that in the clinical setting, too. I don’t think I’ve ever attributed it to prior traumatic brain injury. You’ve answered one of my other questions, which was timing, like can you have a brain injury two decades ago and now have it affect you. I guess one of my questions, because you are in this CCANDL lab and you’re really looking at communication, what does longitudinal decline look like when it comes to a person with these cognitive language changes? What might people actually be experiencing? If you could give us more examples so our listeners know what this might feel like.

He: Yes, the longitudinal decline simply means that the changes we observed when we track a person’s ability over many years. It’s considered a more sensitive measure than a one-time test. In our study, people with a history of TBI showed earlier and faster declines in their language-related ability, like speaking less fluently or finding words more difficult. It’s like aging the brain faster in specific areas, even if overall cognition still seems intact.

Chin: What do these results mean for people who have had a traumatic brain injury but don’t yet have any signs of Alzheimer’s biologically and are not showing cognitive decline? Are they just simply at higher risk?

He: Yes, I think other than the higher risk, the key takeaway for our listeners is awareness and proactive management. This shouldn’t be a cause of panic, but more for empowerment. If you’ve had a significant TBI, it means you should be more attentive to your brain health. It’s a reason to work with your doctor on monitoring your cognitive and language function and to adopt a healthy brain lifestyle, as these protective actions may be even more impactful for a person who experienced TBI.

Chin: Are there scientists who are looking at, because you talked about the controversy, so are there scientists looking at whether or not TBI actually induces amyloid? You talked about acceleration or inducing tau or maybe leading to an earlier onset as to when someone develops amyloid. Are there people looking at the timing of this, or do you know ahead of time now what that relationship might be?

He: Yes, the accumulation of amyloid and tau is a very critical piece for our study with TBI in the context of Alzheimer’s. Some studies have reported that a single moderate to severe TBI can trigger a rapid and acute increase in both amyloid and tau protein in the brain almost immediately after the injury. However, in most of the cases, this clears up and they recover within about three months. The theory is that for others, the injury may last and have a long-term impact. It may prime the brain, making it more vulnerable to the abnormal accumulation of those proteins–again, later in their life–potentially initiating a neurodegenerative process. Which is very different from traditionally how we think of TBI, which is a one-time neurological disease.

Chin: This is fascinating, and it really makes it actually more complicated, the relationship between TBI and Alzheimer’s, which is important for us to figure out. It actually fits into my last question for you, which is always trying to bring it back to us as humans and what we can do to stay as healthy as possible and prevent some of these things. For you, when you explain your research to family and friends, what do you say when they inevitably ask you about ways to reduce the risk of TBI? What are the key tips you tell them? Or if they’ve had a TBI, what do you tell them they should be doing to prevent these future things or delay these future things from happening?

He: Yes, absolutely. TBI is now considered one of the 12 modifiable risks for dementia. First, prevent the injury. This is the most straightforward step. Always wear your seatbelt. Use a proper helmet for activities like biking, skiing or contact sports. For people who are slightly older, make simple home safety changes like removing tripping hazards to prevent falls. Second, respond correctly if injured. This one is crucial. If you hit your head and experience any symptoms like confusion, dizziness or nausea, don’t try to tough it out. See a doctor, get a clear diagnosis and give your brain the time it needs to fully heal before you return to your normal activity. Last, I think it’s very important to build the brain’s resilience. Think of building a cognitive reserve. You can do this by staying socially and mentally active through conversation, reading and learning. These activities directly exercise the neural paths we use for communication and thinking, which can help your brain better withstand challenges later on.

Chin: Well, Deling, that’s a wonderful way to end. Those are fantastic tips, and we’ll have those in our show notes too. Thank you so much for coming on Dementia Matters today, talking about the study you conducted, your presentation at AAIC, and I certainly hope this becomes a publication for you. I think it’s fantastic work, and I look forward to seeing what else is to come.

Outro: Thank you for listening to Dementia Matters. Follow us on Apple Podcasts, Spotify or wherever you listen. Or tell your smart speaker to play the Dementia Matters podcast. Please rate us on your favorite podcast app. It helps other people find our show and lets us know how we’re doing. If you enjoy our show and want to support our work, consider making a gift to the Dementia Matters Fund through the UW Initiative to End Alzheimer’s. All donations go toward outreach and production. Donate at the link in the description. Dementia Matters is brought to you by the Wisconsin Alzheimer’s Disease Research Center at the University of Wisconsin–Madison. It receives funding from private, university, state and national sources, including a grant from the National Institutes on Aging for Alzheimer’s Disease Research. This episode of Dementia Matters was produced by Caoilfhinn Rauwerdink and edited by Alexia Spevacek. Our musical jingle is “Cases to Rest” by Blue Dot Sessions. To learn more about the Wisconsin Alzheimer’s Disease Research Center, check out our website at adrc.wisc.edu. That’s adrc.wisc.edu and follow us on Facebook and Twitter. If you have any questions or comments, email us at Dementia Matters at medicine.wisc.edu. Thanks for listening.