Traumatic Brain Injury and Accelerated Alzheimer's
Traumatic Brain Injury and Accelerated Alzheimer's
This is the Medscape Neurology Minute. I am Dr. Alan Jacobs. There are thought to be epidemiologic and pathophysiologic links between traumatic brain injury (TBI) and Alzheimer disease. Amyloid plaques have been found in the brains of up to 30% of patients who died at any age in the acute phase of a TBI. Now, researchers from the University of Cambridge, England, have published a study in JAMA Neurology in which they performed PET using Pittsburgh Compound B (PiB), a marker of brain amyloid deposition in 15 patients with TBI and 11 healthy control individuals. The patients with TBI were recruited after a maximum of 1 year after injury. They validated their findings using autopsy-acquired brain tissue from 16 TBI victims and 17 patients with nonneurologic causes of death. The results showed that compared with the controls, the patients with TBI showed significantly increased PiB binding throughout the cortical gray matter and the striatum. In the autopsy tissue samples, they found PiB binding in the neocortical gray matter in the same regions where amyloid deposition was demonstrated by immunohistochemistry, thus validating the specificity of the PiB signal to amyloid. The investigators concluded that the use of PiB PET for amyloid imaging following TBI provides the potential for understanding the pathophysiology of TBI, for characterizing the mechanistic drivers of disease progression or suboptimal recovery in the subacute phase of TBI, and for identifying patients at high risk for accelerated Alzheimer disease and for evaluating the potential of antiamyloid therapy. This has been the Medscape Neurology Minute. I'm Dr. Alan Jacobs.
This is the Medscape Neurology Minute. I am Dr. Alan Jacobs. There are thought to be epidemiologic and pathophysiologic links between traumatic brain injury (TBI) and Alzheimer disease. Amyloid plaques have been found in the brains of up to 30% of patients who died at any age in the acute phase of a TBI. Now, researchers from the University of Cambridge, England, have published a study in JAMA Neurology in which they performed PET using Pittsburgh Compound B (PiB), a marker of brain amyloid deposition in 15 patients with TBI and 11 healthy control individuals. The patients with TBI were recruited after a maximum of 1 year after injury. They validated their findings using autopsy-acquired brain tissue from 16 TBI victims and 17 patients with nonneurologic causes of death. The results showed that compared with the controls, the patients with TBI showed significantly increased PiB binding throughout the cortical gray matter and the striatum. In the autopsy tissue samples, they found PiB binding in the neocortical gray matter in the same regions where amyloid deposition was demonstrated by immunohistochemistry, thus validating the specificity of the PiB signal to amyloid. The investigators concluded that the use of PiB PET for amyloid imaging following TBI provides the potential for understanding the pathophysiology of TBI, for characterizing the mechanistic drivers of disease progression or suboptimal recovery in the subacute phase of TBI, and for identifying patients at high risk for accelerated Alzheimer disease and for evaluating the potential of antiamyloid therapy. This has been the Medscape Neurology Minute. I'm Dr. Alan Jacobs.
Source...