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Study Shows Possible Increased Alzheimer’s in Veterans Exposed to Explosive Blasts

Explosive Ordnance Disposal Marines with Special Purpose Marine Air Ground Task Force - Crisis Response - Central Command 16.2, Soldiers with the 797th Ordnance Co., 79th Ordnance Bn., perform combined explosive effects training at an undisclosed location in Southwest Asia, May 10, 2016. Credit: Donald Holdbert

Research shows that Soldiers exposed to shockwaves from military explosives are at a higher risk for developing Alzheimer’s disease — even those that don’t have traumatic brain injuries from those blasts. This new Army-funded study identifies how those blasts affect the brain.

A lead team of experts at UNC Pembroke in collaboration with U.S. Army Research Laboratory and National Institutes of Health scientists authored a study that set out to understand how shockwaves from explosives may lead to an increased risk of Alzheimer’s disease.

The scientific team found that the mystery behind blast-induced neurological complications when traumatic damage is undetected may be rooted in distinct alterations to the tiny connections between neurons in the hippocampus, the part of the brain particularly involved in memory encoding and social behavior.

“Blasts can lead to debilitating neurological and psychological damage but the underlying injury mechanisms are not well understood,” said Dr. Frederick Gregory, program manager, ARO. “Understanding the molecular pathophysiology of blast-induced brain injury and potential impacts on long-term brain health is extremely important to understand in order to protect the lifelong health and well-being of our service members.”

The research team tested slices of rat hippocampus by exposing the healthy tissue to controlled military blast waves. In the experimental brain explants (tissue slices maintained alive in culture dishes), the rapid blast waves produced by the detonated military explosives led to selective reductions in components of brain connections needed for memory, and the distinct electrical activity from those neuronal connections was sharply diminished.

The research showed that the blast-induced effects were evident among healthy neurons with subtle synaptic pathology, which may be an early indicator of Alzheimer’s-type pathogenesis occurring independent of overt brain damage.

“This finding may explain those many blast-exposed individuals returning from war zones with no detectable brain injury, but who still suffer from persistent neurological symptoms, including depression, headaches, irritability and memory problems,” said Dr. Ben Bahr, the William C. Friday distinguished professor of Molecular Biology and Biochemistry at UNC-Pembroke.

“Early detection of this measurable deterioration could improve diagnoses and treatment of recurring neuropsychiatric impediments, and reduce the risk of developing dementia and Alzheimer’s disease later in life,” Bahr said.

Distinct and Dementia-Related Synaptopathy in the Hippocampus after Military Blast Exposures. Brain Pathology, 24 February 2021.

Summary: Explosive blasts account for a majority of the injuries among wounded service members, as hundreds of thousands of veterans from wars of the 21st century are estimated to have experienced brain injuries caused by military or improvised explosives, and signs of neuropathology were found in postmortem brains from veterans that died years after blast exposures. Delayed cellular responses occur due to blast exposure, suggesting that a subset of exposed individuals can have no apparent injury or symptoms, only to experience delayed effects to brain mechanisms and behavioral functions. Those with blast-induced neurotrauma and associated neurological intrusion, but without the typical neuropathology of a TBI, face a major challenge for diagnosis. Neuroimaging techniques are improving but have yet to achieve the level of sensitivity needed to detect subtle blast-induced alterations that underlie lasting neurological impediments. Military blast shockwaves lead to a level of synaptic pathology that is more subtle than mild TBI, perhaps explaining the enhanced dementia risk by initiating Alzheimer-type neuronal compromise. Thus, a key biomarker is one that can identify early synaptic alterations specifically mediated by blast exposure, especially those related to dementia-type synaptopathology. Early detection of measurable synaptopathy may lead to vital improvements in diagnoses, the treatment of recurring neuropsychiatric impediments, and reducing the risk of developing dementia later in life, as the increased risk is likely rooted in the disruptions of synaptic communication instigated by blast exposures.

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