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New Research Shows How Blast Exposure May Cause Alzheimer’s

Blast Exposure May Cause Alzheimer's

.Researchers at the University of Washington School of Medicine and VA Puget Sound Health Care System discovered that American veterans of the wars in Afghanistan and Iraq who suffered from a mild traumatic brain injury from exposure to explosive blasts had abnormalities in cerebrospinal fluid proteins that usually occur in individuals who develop Alzheimer’s. 

A recent study published in the journal Neurology suggests that middle-aged veterans who suffered concussions from blasts from explosive devices might have biomarkers in their spinal fluid similar to those who develop Alzheimer’s [1].

Traumatic brain injury (TBI) is the result of a bump, blow, or jolt to the head, as well as head injuries from falls, car accidents, attacks, blasts, and impact injuries among military personnel.

Mild TBI, often known as a concussion, occurs when a person loses or experiences a disturbance of consciousness. A momentary loss of consciousness might last anywhere from a few seconds to half an hour.

Earlier studies have indicated that having a moderate to severe traumatic brain injury raises an individual’s Alzheimer’s risk [2]. However, it is unclear if a mild traumatic brain injury (mTBI) raises the same kind of risk.

About the Recent Research

In the latest study, researchers examined protein levels in spinal fluid from 51 American veterans of the Afghanistan and Iraq wars. Every individual had sustained multiple blast injuries (mTBIs) as a result of being exposed to explosive blasts. With an average of 20 blast injuries. Researchers compared protein levels with that of 85 individuals who had never experienced a TBI and were civilians of a similar age. 

In this study, soldiers were judged to have sustained a TBI if they experienced an alteration or unconsciousness as a result of the blast. When a typical clinical MRI or CT scan showed no evidence of brain damage and unconsciousness lasted 30 minutes or less, the TBIs were classified as moderate. This type of injury is akin to a concussion.

The researchers assessed protein levels in the veterans’ cerebrospinal fluid (CSF), which circulates through and around the brain and takes away waste substances. The primary building blocks of amyloid plaques, which accumulate in the brains of Alzheimer’s patients, are two of the analyzed proteins. These proteins are alpha-beta amyloid 40 and 42 or Aβ40 and Aβ42. 

The other proteins are variants of the tau protein. Tau proteins are typically present in the cytoskeletons of cells, which give them their shape. However, these structures alter with Alzheimer’s, causing tangles to form within brain cells and ultimately leading to their death. This is another significant characteristic of Alzheimer’s.

What were the Findings?

Alpha-beta amyloid protein levels in spinal fluid usually decline with Alzheimer’s. Researchers speculate that the proteins accumulate in amyloid plaques and stay in the brain. Rather than being flushed out into the spinal fluid and transported away as they typically would. Conversely, as the disease advances, tau levels rise above normal because the proteins are released from dying neurons in the brain.

The study found that mTBI veterans in their late 40s and 50s had lower levels of beta-amyloid proteins than veterans and civilians who had not experienced such injuries.

The older mTBI veterans also had aberrant tau protein levels. Tau levels typically increase with age. However, levels remained constant in older middle-aged mTBI veterans, indicating that the usual brain clearance system may not be working as well in those with mTBI.

In older mTBI veterans, decreased beta-amyloid 42 levels were also linked to worse performance on verbal memory and fluency cognitive tasks.

Senior author Dr. Elaine Peskind, a UW research professor of psychiatry and head of the VA’s Northwest Mental Illness Research, Education, and Clinical Center. Expressed concern about the drop in beta-amyloid proteins, namely beta-amyloid 42.

She stated that a decrease in beta-amyloid 42 is the earliest identifiable. Alzheimer’s-related alteration in a cognitively normal person. The alteration may manifest up to 20 years before any symptoms. Therefore, a person may have the brain pathology associated with Alzheimer’s for up to 20 years without experiencing any symptoms, such as memory loss or cognitive impairment.

Peskind and her colleagues believe that blast-related impairment to the brain’s glymphatic system. Which permits fluids to pass through the brain and remove waste—is the reason for the alterations in the proteins found in the spinal fluid of mTBI veterans.

Alzheimer’s Research Association is a non-profit organization dedicated to helping caregivers of Alzheimer’s disease and dementia. We provide the latest information and news about the illness and helpful tips to help caregivers cope with their daily caregiving challenges. We realize the most important thing that a caregiver needs is financial assistance. Therefore, we provide grants to caregivers to ease their financial burden. Caregivers can apply for grants here: Alzheimer’s Grant Application

You can also help caregivers in their endeavor by donating as much as possible: Donation To Alzheimer’s Research Associations.

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