Traumatic Brain Injury (TBI) & Risk for Dementia

Traumatic brain Injury (TBI) is one of the most well-established risk factors for dementia – importantly, it is modifiable! By reducing the likelihood that you will have a TBI, you can reduce your chance to develop cognitive impairment. So, wear your helmet when you go out for your next bike ride; you can get exercise and protect your brain.

A TBI is caused by a blow or jolt to the head that alters normal brain function, typically measured by a loss of consciousness (getting knocked out). There is no one-to-one association between a single TBI and dementia, including Alzheimer’s disease.

Did you have a concussion (that is, a mild TBI) 50 years ago while you were playing school sports, and now you are worried about dementia? The evidence suggests that that TBI will not cause Alzheimer’s disease directly. People that experience a mild TBI do increase their risk of developing dementia and may develop memory problems at a younger age than people who did not experience a TBI. The greater the severity of a TBI, the greater the risk of developing dementia. The more TBIs that you have, the greater the risk for dementia. Risk is like a lottery, and increasing risk is like buying more lottery tickets – But, it is a lottery you don’t want to win!

Many repeated blows to the head, such as experienced by a boxer, is thought to lead to a degenerative brain disease called chronic traumatic encephalopathy (CTE). It is currently not known how many hits to the head it takes to develop CTE.

Lifestyle changes alone, including helmets, are not enough to prevent all TBIs. Millions of people each year will have a TBI and will visit the hospital’s emergency department. Research at the Sanders-Brown Center on Aging asks what needs to be done to prevent TBI from increasing the risk of developing dementia and doing so at a younger age.  

Work in the Sanders-Brown Center on Aging is investing in research connected to TBI and dementia in the following ways:

1) Selective vulnerability. Does it matter at what age you have a TBI to the likelihood that it will have a long-term effect on your brain? Does a TBI, when you’re a young adult, middle aged, or older adult, affect the brain in the same way? How does genetics, such as APOE, affect your long-term vulnerability to a TBI. What about diet and gut microbiome? These are all areas that are currently being explored by the Sanders-Brown Center on Aging.

2) Therapeutic interventions. There are currently no FDA approved drugs for neuroprotection after a TBI. Unlike much of dementia research where the starting point of the disease is unknown, TBI is different. We know when people have a TBI, and this is potentially a critical point for therapy. At Sanders-Brown Center on Aging, we are developing new therapies targeting inflammation and brain metabolism, among others.  

3) Biological mechanisms. At this point, there is much to be learned about how TBI might interact with dementia. Is a TBI accelerating neurodegenerative pathology leading to dementia, or are there other mechanisms involved? How does a TBI affect glial function, synaptic integrity, and the brain’s barrier and vasculature function? Uncovering the biology of the long-term effect of TBI on the brain is critical for the future of dementia prevention and treatment.

Adam Bachstetter
adam.bachstetter@uky.edu

Address

BB459, BBSRB
741 S Limestone St.
Lexington, KY 40508

Phone Number

(859) 218-4315 (office)

 

Linda Van Eldik
linda.vaneldik@uky.edu

Address

Room 101A, Sanders-Brown
800 S. Limestone Street
Lexington, KY 40536-0230

Phone Number

(859) 257-5566 (office)
(859) 323-2866 (fax)

Josh Morganti
josh.morganti@uky.edu

Address

Room 433, Sanders-Brown
800 S. Limestone Street
Lexington, KY 40536-0230

Phone Number

(859) 257-0398 (office) 

 

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