Perspective from Heather Snyder, PhD
Source/Disclosures
Source: Mohammed AZ, et al. Traumatic Brain Injury May Fast-Forwards Alzheimer’s Pathology: Evidence from Amyloid PET. Presented at: The Alzheimer's Association International Conference Neuroscience Next. Nov. 9-10, 2020 (virtual meeting).

Disclosures: Healio Primary Care was unable to confirm relevant financial disclosures at the time of publication.
December 02, 2020
2 min read
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TBI ‘significantly fast-forwards’ clinical onset of Alzheimer’s disease

Perspective from Heather Snyder, PhD
Source/Disclosures
Source: Mohammed AZ, et al. Traumatic Brain Injury May Fast-Forwards Alzheimer’s Pathology: Evidence from Amyloid PET. Presented at: The Alzheimer's Association International Conference Neuroscience Next. Nov. 9-10, 2020 (virtual meeting).

Disclosures: Healio Primary Care was unable to confirm relevant financial disclosures at the time of publication.
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Patients with a history of traumatic brain injury experienced the clinical onset of Alzheimer’s disease several years earlier than those without TBI, data show.

The findings, presented at the virtual Alzheimer's Association International Conference Neuroscience Next, showed that a history of TBI was associated with “higher amyloid deposition and cognitive deficit” in patients with Alzheimer’s disease (AD), researchers reported.

“Increased amyloid-plaque build-up in the brain triggered by a traumatic brain injury plays an important role in the development of the pathology and symptoms associated with Alzheimer’s disease.”  The source of the quote is: Abdalla Z. Mohamed, post-doctorate fellow.

“While this study does not directly shed light on the mechanisms tying TBI to AD, it clearly shows that increased amyloid-plaque build-up in the brain triggered by a traumatic brain injury plays an important role in the development of the pathology and symptoms associated with AD,” Abdalla Z. Mohamed, a post-doctorate fellow at the University of Sunshine Coast’s Mind and Neuroscience Thompson Institute, told Healio Primary Care.

The data could be used to help identify patients at higher risk for developing AD, he added.

“The expression of [AD’s] main pathological features, including the accumulation of -amyloid plaques, tau aggregates and angles and neural loss may initiate years to decades prior to the onset of obvious clinical symptoms,” Mohamed said. “Introducing a method to identify pre-symptomology biomarkers and pathologies early in the populations with risk for Alzheimer’s disease, thus expanding the therapeutic window, might enable timely interventions that alter or mitigate against the course of the disease.”

In what Mohamed called the first study of its kind, he and his colleagues analyzed 241 amyloid positron emission tomography scans from the Alzheimer’s Disease Neuroimaging Initiative public database to look for differences in standardized uptake value ratio, cortical morphometry and neuropsychological assessments. Though the scans came from patients aged 65 years and older, these patients’ clinical dementia ratings and TBI histories varied.

Mohamed and colleagues wrote that the scans indicating TBI and a clinical dementia rating score of 0.5 or higher were associated with an earlier age of onset of cognitive impairment (P = .005) vs. the scans with no TBI and similar clinical dementia ratings, indicating TBI “significantly fast-forwards the age of clinical onset of AD by approximately 4 years.” In addition, amyloid-positive scans with earlier TBI showed higher amyloid deposition and brain atrophy at the hippocampus as well as parietal, cingulate, frontal and temporal cortices vs. nonamyloid-positive scans. A comparison between amyloid-positive participants with and without TBI and clinical dementia ratings of 0.5 or higher, with matching for Mini-Mental State Exam scores, revealed greater amyloid burden and earlier onset of cognitive impairments in those with a history of TBI.