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Brain Trauma and Alzheimer’s

Historically, there has been an association between brain injury and the later development of Alzheimer’s. The research regarding persons who have suffered repetitive trauma (boxers or football players) is clear – that repetitive trauma gives rise to the devastating condition known as Chronic Traumatic Encephalopathy, which is in effect, ultra early Alzheimer’s (U. EAD). In recent autopsies of deceased football players, pathologists encountered brains which appeared to be the brains of elderly people, when in fact the individuals were in their 30’s or 40’s. The repetitive trauma creates an accumulation of amyloid plaque and later “tangles” known as intracellular neurofibrillary threads (NFT) which are the hallmarks of this condition.

 

It was speculated, but not proven by any study, that a similar development could occur in the brain after a single traumatic brain injury in humans. Now, a recent study (Johnson VE et al. 2012) has shown that in those with a history of a single traumatic brain injury, there is long term pathology, involving a greater density of amyloid plaques and widespread NFT, in a third of the patients followed with survival of a year or more. The authors noted “This suggests that a single TBI induces long term neuropathologic changes akin to those found in neuro-degenerative disease.” Another study published in Brain Pathology (Chen X et al., 2009) followed 23 cases of post TBI survival patients for three years and found that even years later there was continued neuronal swelling in the axonal bulbs and axons. Strangely, the degree of axonal pathology three years later in survivors was higher than the cases in which death occurred after a much shorter duration, showing that axons continued to swell and disconnect over a protracted period of time. They noted “that the” at persistent nature of this pathology suggests that TBI can induce a progressive neuro-degenerative process.” The final mystery was that in this study, unlike some others, they did not find accumulation of amyloid plaque years later, even in the face of ongoing degeneration of brain tissue.

This news adds the our already staggering burden of future Alzheimer’s victims. To add thousands of additional individuals a year, because of TBI, to the pool of likely or even possible Alzheimer’s victims is distressing. We can only hope that our politicians and leaders in healthcare are taking notice of this potential time bomb. Add in injured soldiers and those unknowingly injured by repetitive trauma in a lifetime of sports and the future need for an Alzheimer’s cure becomes almost imperative.

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