Amyloid plaques in TBI Incidental finding or precursor for what is to come?

摘要

Over the past decade, the rate of traumatic brain injury (TBI)-related emergency department visits has increased by 70% and was estimated in 2010 at a staggering 2.5 million visits. This number is an underestimate as it does not include individuals who did not seek/receive medical care, are part of the US military service, or cared for by the Department of Veterans Affairs. One estimate states that 3 to 5 million Americans live with a TBI-related disability.(1) Of particular concern, recent data suggest an increased risk of dementia after TBI. However, it remains unclear whether there is indeed a specific link between the occurrence of Alzheimer disease (AD) later in life and a history of TBI. The suspicion of a causal relationship between TBI and AD mostly stems from the sudden emergence of the toxic beta-amyloid (A beta) protein observed in the brains of even young patients. This finding has been puzzling, as A beta is a hallmark of AD, a late-life dementia. Whether the primarily axonal increase of A beta is simply an epiphenomenon of TBI pathology or actually a precursor to the distinctively different extraneuronal fibrillar A beta plaques seen in AD remains elusive.