Biomedical Research

Preventing Nerve Cell Deterioration After Traumatic Brain Injury

Traumatic brain injuries are quite common in the US and cause a multitude of neurological conditions. A research team in Ohio discovered two possible treatments for traumatic brain injury and preventing Alzheimer’s disease as well.

By Kyle Phong

Published 1:46 PM EST, Sat May 15, 2021


Traumatic brain injury (TBI) is often caused by a blow to the head and currently affects around five million people across the US. It is known to cause several neuropsychiatric conditions such as psychosis, mania, and Alzheimer’s disease, and can also lead to nerve cell deterioration. At the Harrington Discovery Institute in Cleveland, Ohio, Dr. Pieper and his team have discovered a way to prevent TBI-induced nerve cell deterioration in the brain.  They also found a possible explanation for the relationship between TBI and Alzheimer’s disease.

Osmosis, “Traumatic Brain Injury (TBI)” 


To explore the connection between Alzheimer’s and TBI, Dr. Pieper used previous knowledge of tau and acetylation in patients.  Tau is a protein in nerve cells that help guide nutrients throughout the neuron.  However, tau tangles with other tau molecules in patients with Alzheimer’s disease, resulting in weak synaptic communication between neurons and becoming acetylated-tau.  While experimenting with mice, Dr. Pieper found high levels of acetylated-tau (ac-tau) in different forms of TBI.  The elevated ac-tau persisted chronically if left without treatment.  Furthermore, patients with Alzheimer’s disease had even higher levels of ac-tau if they had a history of TBI.

Labiotech, “Healthy Neuron vs Alzheimer’s Disease Neuron”

Dr. Pieper’s team found two anti-inflammatory drugs (salsalate and diflunisal) that helped to protect the mice’s neurons from deteriorating after TBI.  These two medications inhibit the enzyme that causes tau acetylation, therefore preventing the transformation into ac-tau.  Upon this discovery, the researchers analyzed over seven million patient records regarding the usage of salsalate and diflunisal and realized that these medications were associated with a decrease in Alzheimer’s disease and TBI cases.  Additionally, they compared these two drugs with aspirin, a common anti-inflammatory drug, that does not prevent acetylation.  Dr. Pieper did not find any evidence of aspirin showing the same neuroprotective activity as salsalate and diflunisal.

Knowing that tau is a protein that diffuses from the brain into the bloodstream, the researchers wondered about ac-tau levels existing in the blood of TBI patients.  For both mice and humans, there was a significant increase of ac-tau in the blood.  However, these elevated levels returned to normal when treated with medications such as salsalate and diflunisal, showing again that they effectively protect nerve cells from deterioration. 


Dr. Rosa, the co-author of this study, explains that this newfound knowledge can have a variety of uses in the clinical setting.  The research team is continuing to examine ac-tau and its relationship with neurodegenerative diseases.  Additionally, they will study salsalate and diflunisal to see whether these drugs can be used as an established neuroprotective medication for humans. 

Kyle Phong, Youth Medical Journal 2021


News Medical Life Sciences, “Researchers discover a new way to prevent brain nerve cells from deteriorating after injury”, 13 April 2021

Cell, “Reducing acetylated tau is neuroprotective in brain injury”, 13 April 2021

Osmosis, “Traumatic brain injury: Clinical practice” Image

Labiotech, “How AC Immune CEO Andrea Pfiefer is Tackling Alzheimer’s Disease” Image, 1 August 2018


By Kyle Phong

Kyle Phong is a student at Whitney High School in Cerritos, California. He enjoys learning about the fields of psychology and evolution.

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